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Apolipoproteins EApolipoproteins CApolipoproteinsApolipoprotein C-IIIApolipoprotein E3Apolipoproteins ALipoproteinsApolipoproteins BApolipoprotein A-IApolipoprotein A-IIApolipoprotein C-IILipoproteins, HDLApolipoproteins DApolipoprotein C-ICholesterolLipoproteins, VLDLTriglyceridesLipidsApolipoprotein B-100Apolipoprotein B-48Cholesterol, HDLLipoproteins, HDL3Tangier DiseasePhosphatidylcholine-Sterol O-AcyltransferaseLipoproteins, LDLNephelometry and TurbidimetryATP Binding Cassette Transporter 1Cholesterol EstersIsoelectric FocusingReceptors, LipoproteinLipid MetabolismChylomicronsCholesterol, LDLPhospholipidsUltracentrifugationHypolipoproteinemiasLipoproteins, HDL2Lipoprotein(a)LymphElectrophoresis, Polyacrylamide GelApoproteinsHyperlipidemiasLiverImmunodiffusionLipoprotein LipaseTrioleinHyperlipoproteinemia Type IVPhosphatidylcholinesKineticsATP-Binding Cassette TransportersHyperlipoproteinemiasChemistry, ClinicalCholesterol, VLDLHypertriglyceridemiaCholesterol Ester Transfer ProteinsLipoproteins, IDLReference ValuesScavenger Receptors, Class BFreeze DryingEthinyl EstradiolParticle SizeImmunoassaySerum Amyloid A ProteinDietary FatsMicroscopy, ElectronImmunoelectrophoresisHyperlipoproteinemia Type VAbetalipoproteinemiaDimyristoylphosphatidylcholineReceptors, ScavengerAmino Acid SequenceOleic AcidChromatography, GelMolecular WeightArteriosclerosisBiological TransportLipolysisSterol O-AcyltransferaseRats, Inbred StrainsCallitrichinaeHigh-Density Lipoproteins, Pre-betaLipaseLiposomesReceptors, LDLOleic AcidsCarrier ProteinsMolecular Sequence DataLecithin Acyltransferase DeficiencyHyperlipidemia, Familial CombinedProtein BindingAntigens, CD36
Apolipoproteins E: A class of protein components which can be found in several lipoproteins including HIGH-DENSITY LIPOPROTEINS; VERY-LOW-DENSITY LIPOPROTEINS; and CHYLOMICRONS. Synthesized in most organs, Apo E is important in the global transport of lipids and cholesterol throughout the body. Apo E is also a ligand for LDL receptors (RECEPTORS, LDL) that mediates the binding, internalization, and catabolism of lipoprotein particles in cells. There are several allelic isoforms (such as E2, E3, and E4). Deficiency or defects in Apo E are causes of HYPERLIPOPROTEINEMIA TYPE III.Apolipoproteins C: A group of apolipoproteins that can readily exchange among the various classes of lipoproteins (HDL; VLDL; CHYLOMICRONS). After lipolysis of TRIGLYCERIDES on VLDL and chylomicrons, Apo-C proteins are normally transferred to HDL. The subtypes can modulate remnant binding to receptors, LECITHIN CHOLESTEROL ACYLTRANSFERASE, or LIPOPROTEIN LIPASE.Apolipoproteins: Protein components on the surface of LIPOPROTEINS. They form a layer surrounding the hydrophobic lipid core. There are several classes of apolipoproteins with each playing a different role in lipid transport and LIPID METABOLISM. These proteins are synthesized mainly in the LIVER and the INTESTINES.Apolipoprotein C-III: A 9-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS and CHYLOMICRON REMNANTS. Apo C-III, synthesized in the liver, is an inhibitor of LIPOPROTEIN LIPASE. Apo C-III modulates the binding of chylomicron remnants and VLDL to receptors (RECEPTORS, LDL) thus decreases the uptake of triglyceride-rich particles by the liver cells and subsequent degradation. The normal Apo C-III is glycosylated. There are several polymorphic forms with varying amounts of SIALIC ACID (Apo C-III-0, Apo C-III-1, and Apo C-III-2).Apolipoprotein E3: A 34-kDa glycosylated protein. A major and most common isoform of apolipoprotein E. Therefore, it is also known as apolipoprotein E (ApoE). In human, Apo E3 is a 299-amino acid protein with a cysteine at the 112 and an arginine at the 158 position. It is involved with the transport of TRIGLYCERIDES; PHOSPHOLIPIDS; CHOLESTEROL; and CHOLESTERYL ESTERS in and out of the cells.Apolipoproteins A: Structural proteins of the alpha-lipoproteins (HIGH DENSITY LIPOPROTEINS), including APOLIPOPROTEIN A-I and APOLIPOPROTEIN A-II. They can modulate the activity of LECITHIN CHOLESTEROL ACYLTRANSFERASE. These apolipoproteins are low in atherosclerotic patients. They are either absent or present in extremely low plasma concentration in TANGIER DISEASE.Lipoproteins: Lipid-protein complexes involved in the transportation and metabolism of lipids in the body. They are spherical particles consisting of a hydrophobic core of TRIGLYCERIDES and CHOLESTEROL ESTERS surrounded by a layer of hydrophilic free CHOLESTEROL; PHOSPHOLIPIDS; and APOLIPOPROTEINS. Lipoproteins are classified by their varying buoyant density and sizes.Apolipoproteins B: Major structural proteins of triacylglycerol-rich LIPOPROTEINS. There are two forms, apolipoprotein B-100 and apolipoprotein B-48, both derived from a single gene. ApoB-100 expressed in the liver is found in low-density lipoproteins (LIPOPROTEINS, LDL; LIPOPROTEINS, VLDL). ApoB-48 expressed in the intestine is found in CHYLOMICRONS. They are important in the biosynthesis, transport, and metabolism of triacylglycerol-rich lipoproteins. Plasma Apo-B levels are high in atherosclerotic patients but non-detectable in ABETALIPOPROTEINEMIA.Apolipoprotein A-I: The most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. This protein serves as an acceptor for CHOLESTEROL released from cells thus promoting efflux of cholesterol to HDL then to the LIVER for excretion from the body (reverse cholesterol transport). It also acts as a cofactor for LECITHIN CHOLESTEROL ACYLTRANSFERASE that forms CHOLESTEROL ESTERS on the HDL particles. Mutations of this gene APOA1 cause HDL deficiency, such as in FAMILIAL ALPHA LIPOPROTEIN DEFICIENCY DISEASE and in some patients with TANGIER DISEASE.Apolipoprotein A-II: The second most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. It has a high lipid affinity and is known to displace APOLIPOPROTEIN A-I from HDL particles and generates a stable HDL complex. ApoA-II can modulate the activation of LECITHIN CHOLESTEROL ACYLTRANSFERASE in the presence of APOLIPOPROTEIN A-I, thus affecting HDL metabolism.Apolipoprotein C-II: A 9-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS. It contains a cofactor for LIPOPROTEIN LIPASE and activates several triacylglycerol lipases. The association of Apo C-II with plasma CHYLOMICRONS; VLDL, and HIGH-DENSITY LIPOPROTEINS is reversible and changes rapidly as a function of triglyceride metabolism. Clinically, Apo C-II deficiency is similar to lipoprotein lipase deficiency (HYPERLIPOPROTEINEMIA TYPE I) and is therefore called hyperlipoproteinemia type IB.Lipoproteins, HDL: A class of lipoproteins of small size (4-13 nm) and dense (greater than 1.063 g/ml) particles. HDL lipoproteins, synthesized in the liver without a lipid core, accumulate cholesterol esters from peripheral tissues and transport them to the liver for re-utilization or elimination from the body (the reverse cholesterol transport). Their major protein component is APOLIPOPROTEIN A-I. HDL also shuttle APOLIPOPROTEINS C and APOLIPOPROTEINS E to and from triglyceride-rich lipoproteins during their catabolism. HDL plasma level has been inversely correlated with the risk of cardiovascular diseases.Apolipoproteins D: A glycoprotein component of HIGH-DENSITY LIPOPROTEINS that transports small hydrophobic ligands including CHOLESTEROL and STEROLS. It occurs in the macromolecular complex with LECITHIN CHOLESTEROL ACYLTRANSFERASE. Apo D is expressed in and secreted from a variety of tissues such as liver, placenta, brain tissue and others.Apolipoprotein C-I: A 6.6-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS; INTERMEDIATE-DENSITY LIPOPROTEINS; and HIGH-DENSITY LIPOPROTEINS. Apo C-I displaces APO E from lipoproteins, modulate their binding to receptors (RECEPTORS, LDL), and thereby decrease their clearance from plasma. Elevated Apo C-I levels are associated with HYPERLIPOPROTEINEMIA and ATHEROSCLEROSIS.Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.Lipoproteins, VLDL: A class of lipoproteins of very light (0.93-1.006 g/ml) large size (30-80 nm) particles with a core composed mainly of TRIGLYCERIDES and a surface monolayer of PHOSPHOLIPIDS and CHOLESTEROL into which are imbedded the apolipoproteins B, E, and C. VLDL facilitates the transport of endogenously made triglycerides to extrahepatic tissues. As triglycerides and Apo C are removed, VLDL is converted to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LOW-DENSITY LIPOPROTEINS from which cholesterol is delivered to the extrahepatic tissues.TriglyceridesLipids: A generic term for fats and lipoids, the alcohol-ether-soluble constituents of protoplasm, which are insoluble in water. They comprise the fats, fatty oils, essential oils, waxes, phospholipids, glycolipids, sulfolipids, aminolipids, chromolipids (lipochromes), and fatty acids. (Grant & Hackh's Chemical Dictionary, 5th ed)Apolipoprotein B-100: A 513-kDa protein synthesized in the LIVER. It serves as the major structural protein of low-density lipoproteins (LIPOPROTEINS, LDL; LIPOPROTEINS, VLDL). It is the ligand for the LDL receptor (RECEPTORS, LDL) that promotes cellular binding and internalization of LDL particles.Apolipoprotein B-48: A 241-kDa protein synthesized only in the INTESTINES. It serves as a structural protein of CHYLOMICRONS. Its exclusive association with chylomicron particles provides an indicator of intestinally derived lipoproteins in circulation. Apo B-48 is a shortened form of apo B-100 and lacks the LDL-receptor region.Cholesterol, HDL: Cholesterol which is contained in or bound to high-density lipoproteins (HDL), including CHOLESTEROL ESTERS and free cholesterol.Lipoproteins, HDL3: Intermediate-density subclass of the high-density lipoproteins, with particle sizes between 7 to 8 nm. As the larger lighter HDL2 lipoprotein, HDL3 lipoprotein is lipid-rich.Tangier Disease: An autosomal recessively inherited disorder caused by mutation of ATP-BINDING CASSETTE TRANSPORTERS involved in cellular cholesterol removal (reverse-cholesterol transport). It is characterized by near absence of ALPHA-LIPOPROTEINS (high-density lipoproteins) in blood. The massive tissue deposition of cholesterol esters results in HEPATOMEGALY; SPLENOMEGALY; RETINITIS PIGMENTOSA; large orange tonsils; and often sensory POLYNEUROPATHY. The disorder was first found among inhabitants of Tangier Island in the Chesapeake Bay, MD.Phosphatidylcholine-Sterol O-Acyltransferase: An enzyme secreted from the liver into the plasma of many mammalian species. It catalyzes the esterification of the hydroxyl group of lipoprotein cholesterol by the transfer of a fatty acid from the C-2 position of lecithin. In familial lecithin:cholesterol acyltransferase deficiency disease, the absence of the enzyme results in an excess of unesterified cholesterol in plasma. EC 2.3.1.43.Lipoproteins, LDL: A class of lipoproteins of small size (18-25 nm) and light (1.019-1.063 g/ml) particles with a core composed mainly of CHOLESTEROL ESTERS and smaller amounts of TRIGLYCERIDES. The surface monolayer consists mostly of PHOSPHOLIPIDS, a single copy of APOLIPOPROTEIN B-100, and free cholesterol molecules. The main LDL function is to transport cholesterol and cholesterol esters to extrahepatic tissues.Nephelometry and Turbidimetry: Chemical analysis based on the phenomenon whereby light, passing through a medium with dispersed particles of a different refractive index from that of the medium, is attenuated in intensity by scattering. In turbidimetry, the intensity of light transmitted through the medium, the unscattered light, is measured. In nephelometry, the intensity of the scattered light is measured, usually, but not necessarily, at right angles to the incident light beam.ATP Binding Cassette Transporter 1: A superfamily of large integral ATP-binding cassette membrane proteins whose expression pattern is consistent with a role in lipid (cholesterol) efflux. It is implicated in TANGIER DISEASE characterized by accumulation of cholesteryl ester in various tissues.Cholesterol Esters: Fatty acid esters of cholesterol which constitute about two-thirds of the cholesterol in the plasma. The accumulation of cholesterol esters in the arterial intima is a characteristic feature of atherosclerosis.Isoelectric Focusing: Electrophoresis in which a pH gradient is established in a gel medium and proteins migrate until they reach the site (or focus) at which the pH is equal to their isoelectric point.Receptors, Lipoprotein: Cell surface proteins that bind lipoproteins with high affinity. Lipoprotein receptors in the liver and peripheral tissues mediate the regulation of plasma and cellular cholesterol metabolism and concentration. The receptors generally recognize the apolipoproteins of the lipoprotein complex, and binding is often a trigger for endocytosis.Lipid Metabolism: Physiological processes in biosynthesis (anabolism) and degradation (catabolism) of LIPIDS.Chylomicrons: A class of lipoproteins that carry dietary CHOLESTEROL and TRIGLYCERIDES from the SMALL INTESTINE to the tissues. Their density (0.93-1.006 g/ml) is the same as that of VERY-LOW-DENSITY LIPOPROTEINS.Cholesterol, LDL: Cholesterol which is contained in or bound to low density lipoproteins (LDL), including CHOLESTEROL ESTERS and free cholesterol.Phospholipids: Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides see GLYCEROPHOSPHOLIPIDS) or sphingosine (SPHINGOLIPIDS). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system.Ultracentrifugation: Centrifugation with a centrifuge that develops centrifugal fields of more than 100,000 times gravity. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)Hypolipoproteinemias: Conditions with abnormally low levels of LIPOPROTEINS in the blood. This may involve any of the lipoprotein subclasses, including ALPHA-LIPOPROTEINS (high-density lipoproteins); BETA-LIPOPROTEINS (low-density lipoproteins); and PREBETA-LIPOPROTEINS (very-low-density lipoproteins).Lipoproteins, HDL2: Low-density subclass of the high-density lipoproteins, with particle sizes between 8 to 13 nm.Lipoprotein(a): A lipoprotein that resembles the LOW-DENSITY LIPOPROTEINS but with an extra protein moiety, APOPROTEIN (A) also known as APOLIPOPROTEIN (A), linked to APOLIPOPROTEIN B-100 on the LDL by one or two disulfide bonds. High plasma level of lipoprotein (a) is associated with increased risk of atherosclerotic cardiovascular disease.Lymph: The interstitial fluid that is in the LYMPHATIC SYSTEM.Electrophoresis, Polyacrylamide Gel: Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.Apoproteins: The protein components of a number of complexes, such as enzymes (APOENZYMES), ferritin (APOFERRITINS), or lipoproteins (APOLIPOPROTEINS).Hyperlipidemias: Conditions with excess LIPIDS in the blood.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.Immunodiffusion: Technique involving the diffusion of antigen or antibody through a semisolid medium, usually agar or agarose gel, with the result being a precipitin reaction.Lipoprotein Lipase: An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. The enzyme hydrolyzes triacylglycerols in chylomicrons, very-low-density lipoproteins, low-density lipoproteins, and diacylglycerols. It occurs on capillary endothelial surfaces, especially in mammary, muscle, and adipose tissue. Genetic deficiency of the enzyme causes familial hyperlipoproteinemia Type I. (Dorland, 27th ed) EC 3.1.1.34.Triolein: (Z)-9-Octadecenoic acid 1,2,3-propanetriyl ester.Hyperlipoproteinemia Type IV: A hypertriglyceridemia disorder, often with autosomal dominant inheritance. It is characterized by the persistent elevations of plasma TRIGLYCERIDES, endogenously synthesized and contained predominantly in VERY-LOW-DENSITY LIPOPROTEINS (pre-beta lipoproteins). In contrast, the plasma CHOLESTEROL and PHOSPHOLIPIDS usually remain within normal limits.Phosphatidylcholines: Derivatives of phosphatidic acids in which the phosphoric acid is bound in ester linkage to a choline moiety. Complete hydrolysis yields 1 mole of glycerol, phosphoric acid and choline and 2 moles of fatty acids.Kinetics: The rate dynamics in chemical or physical systems.ATP-Binding Cassette Transporters: A family of MEMBRANE TRANSPORT PROTEINS that require ATP hydrolysis for the transport of substrates across membranes. The protein family derives its name from the ATP-binding domain found on the protein.Hyperlipoproteinemias: Conditions with abnormally elevated levels of LIPOPROTEINS in the blood. They may be inherited, acquired, primary, or secondary. Hyperlipoproteinemias are classified according to the pattern of lipoproteins on electrophoresis or ultracentrifugation.Chemistry, Clinical: The specialty of ANALYTIC CHEMISTRY applied to assays of physiologically important substances found in blood, urine, tissues, and other biological fluids for the purpose of aiding the physician in making a diagnosis or following therapy.Cholesterol, VLDL: Cholesterol which is contained in or bound to very low density lipoproteins (VLDL). High circulating levels of VLDL cholesterol are found in HYPERLIPOPROTEINEMIA TYPE IIB. The cholesterol on the VLDL is eventually delivered by LOW-DENSITY LIPOPROTEINS to the tissues after the catabolism of VLDL to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LDL.Hypertriglyceridemia: A condition of elevated levels of TRIGLYCERIDES in the blood.Cholesterol Ester Transfer Proteins: Proteins that bind to and transfer CHOLESTEROL ESTERS between LIPOPROTEINS such as LOW-DENSITY LIPOPROTEINS and HIGH-DENSITY LIPOPROTEINS.Lipoproteins, IDL: A mixture of very-low-density lipoproteins (VLDL), particularly the triglyceride-poor VLDL, with slow diffuse electrophoretic mobilities in the beta and alpha2 regions which are similar to that of beta-lipoproteins (LDL) or alpha-lipoproteins (HDL). They can be intermediate (remnant) lipoproteins in the de-lipidation process, or remnants of mutant CHYLOMICRONS and VERY-LOW-DENSITY LIPOPROTEINS which cannot be metabolized completely as seen in FAMILIAL DYSBETALIPOPROTEINEMIA.Reference Values: The range or frequency distribution of a measurement in a population (of organisms, organs or things) that has not been selected for the presence of disease or abnormality.Scavenger Receptors, Class B: A family of scavenger receptors that are predominately localized to CAVEOLAE of the PLASMA MEMBRANE and bind HIGH DENSITY LIPOPROTEINS.Freeze Drying: Method of tissue preparation in which the tissue specimen is frozen and then dehydrated at low temperature in a high vacuum. This method is also used for dehydrating pharmaceutical and food products.Ethinyl Estradiol: A semisynthetic alkylated ESTRADIOL with a 17-alpha-ethinyl substitution. It has high estrogenic potency when administered orally, and is often used as the estrogenic component in ORAL CONTRACEPTIVES.Particle Size: Relating to the size of solids.Immunoassay: A technique using antibodies for identifying or quantifying a substance. Usually the substance being studied serves as antigen both in antibody production and in measurement of antibody by the test substance.Serum Amyloid A Protein: An ACUTE PHASE REACTION protein present in low concentrations in normal sera, but found at higher concentrations in sera of older persons and in patients with AMYLOIDOSIS. It is the circulating precusor of amyloid A protein, which is found deposited in AA type AMYLOID FIBRILS.Dietary Fats: Fats present in food, especially in animal products such as meat, meat products, butter, ghee. They are present in lower amounts in nuts, seeds, and avocados.Microscopy, Electron: Microscopy using an electron beam, instead of light, to visualize the sample, thereby allowing much greater magnification. The interactions of ELECTRONS with specimens are used to provide information about the fine structure of that specimen. In TRANSMISSION ELECTRON MICROSCOPY the reactions of the electrons that are transmitted through the specimen are imaged. In SCANNING ELECTRON MICROSCOPY an electron beam falls at a non-normal angle on the specimen and the image is derived from the reactions occurring above the plane of the specimen.Immunoelectrophoresis: A technique that combines protein electrophoresis and double immunodiffusion. In this procedure proteins are first separated by gel electrophoresis (usually agarose), then made visible by immunodiffusion of specific antibodies. A distinct elliptical precipitin arc results for each protein detectable by the antisera.Hyperlipoproteinemia Type V: A severe type of hyperlipidemia, sometimes familial, that is characterized by the elevation of both plasma CHYLOMICRONS and TRIGLYCERIDES contained in VERY-LOW-DENSITY LIPOPROTEINS. Type V hyperlipoproteinemia is often associated with DIABETES MELLITUS and is not caused by reduced LIPOPROTEIN LIPASE activity as in HYPERLIPOPROTEINEMIA TYPE I .Abetalipoproteinemia: An autosomal recessive disorder of lipid metabolism. It is caused by mutation of the microsomal triglyceride transfer protein that catalyzes the transport of lipids (TRIGLYCERIDES; CHOLESTEROL ESTERS; PHOSPHOLIPIDS) and is required in the secretion of BETA-LIPOPROTEINS (low density lipoproteins or LDL). Features include defective intestinal lipid absorption, very low serum cholesterol level, and near absent LDL.Dimyristoylphosphatidylcholine: A synthetic phospholipid used in liposomes and lipid bilayers for the study of biological membranes.Receptors, Scavenger: A large group of structurally diverse cell surface receptors that mediate endocytic uptake of modified LIPOPROTEINS. Scavenger receptors are expressed by MYELOID CELLS and some ENDOTHELIAL CELLS, and were originally characterized based on their ability to bind acetylated LOW-DENSITY LIPOPROTEINS. They can also bind a variety of other polyanionic ligand. Certain scavenger receptors can internalize micro-organisms as well as apoptotic cells.Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.Oleic Acid: An unsaturated fatty acid that is the most widely distributed and abundant fatty acid in nature. It is used commercially in the preparation of oleates and lotions, and as a pharmaceutical solvent. (Stedman, 26th ed)Chromatography, Gel: Chromatography on non-ionic gels without regard to the mechanism of solute discrimination.Molecular Weight: The sum of the weight of all the atoms in a molecule.Arteriosclerosis: Thickening and loss of elasticity of the walls of ARTERIES of all sizes. There are many forms classified by the types of lesions and arteries involved, such as ATHEROSCLEROSIS with fatty lesions in the ARTERIAL INTIMA of medium and large muscular arteries.Biological Transport: The movement of materials (including biochemical substances and drugs) through a biological system at the cellular level. The transport can be across cell membranes and epithelial layers. It also can occur within intracellular compartments and extracellular compartments.Lipolysis: The metabolic process of breaking down LIPIDS to release FREE FATTY ACIDS, the major oxidative fuel for the body. Lipolysis may involve dietary lipids in the DIGESTIVE TRACT, circulating lipids in the BLOOD, and stored lipids in the ADIPOSE TISSUE or the LIVER. A number of enzymes are involved in such lipid hydrolysis, such as LIPASE and LIPOPROTEIN LIPASE from various tissues.Sterol O-Acyltransferase: An enzyme that catalyzes the formation of cholesterol esters by the direct transfer of the fatty acid group from a fatty acyl CoA derivative. This enzyme has been found in the adrenal gland, gonads, liver, intestinal mucosa, and aorta of many mammalian species. EC 2.3.1.26.Rats, Inbred Strains: Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.Callitrichinae: A subfamily in the family CEBIDAE that consists of four genera: CALLITHRIX (marmosets), CALLIMICO (Goeldi's monkey), LEONTOPITHECUS (lion tamarins), and SAGUINUS (long-tusked tamarins). The members of this family inhabit the tropical forests of South and Central America.High-Density Lipoproteins, Pre-beta: A highly dense subclass of the high-density lipoproteins, with particle sizes below 7 nm. They are also known as nascent HDL, composed of a few APOLIPOPROTEIN A-I molecules which are complexed with PHOSPHOLIPIDS. The lipid-poor pre-beta-HDL particles serve as progenitors of HDL3 and then HDL2 after absorption of free cholesterol from cell membranes, cholesterol esterification, and acquisition of apolipoproteins A-II, Cs, and E. Pre-beta-HDL initiate the reverse cholesterol transport process from cells to liver.Lipase: An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. It is produced by glands on the tongue and by the pancreas and initiates the digestion of dietary fats. (From Dorland, 27th ed) EC 3.1.1.3.Liposomes: Artificial, single or multilaminar vesicles (made from lecithins or other lipids) that are used for the delivery of a variety of biological molecules or molecular complexes to cells, for example, drug delivery and gene transfer. They are also used to study membranes and membrane proteins.Receptors, LDL: Receptors on the plasma membrane of nonhepatic cells that specifically bind LDL. The receptors are localized in specialized regions called coated pits. Hypercholesteremia is caused by an allelic genetic defect of three types: 1, receptors do not bind to LDL; 2, there is reduced binding of LDL; and 3, there is normal binding but no internalization of LDL. In consequence, entry of cholesterol esters into the cell is impaired and the intracellular feedback by cholesterol on 3-hydroxy-3-methylglutaryl CoA reductase is lacking.Oleic Acids: A group of fatty acids that contain 18 carbon atoms and a double bond at the omega 9 carbon.Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes.Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.Lecithin Acyltransferase Deficiency: An autosomal recessively inherited disorder caused by mutation of LECITHIN CHOLESTEROL ACYLTRANSFERASE that facilitates the esterification of lipoprotein cholesterol and subsequent removal from peripheral tissues to the liver. This defect results in low HDL-cholesterol level in blood and accumulation of free cholesterol in tissue leading to a triad of CORNEAL OPACITY, hemolytic anemia (ANEMIA, HEMOLYTIC), and PROTEINURIA.Hyperlipidemia, Familial Combined: A type of familial lipid metabolism disorder characterized by a variable pattern of elevated plasma CHOLESTEROL and/or TRIGLYCERIDES. Multiple genes on different chromosomes may be involved, such as the major late transcription factor (UPSTREAM STIMULATORY FACTORS) on CHROMOSOME 1.Protein Binding: The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.Antigens, CD36: Leukocyte differentiation antigens and major platelet membrane glycoproteins present on MONOCYTES; ENDOTHELIAL CELLS; PLATELETS; and mammary EPITHELIAL CELLS. They play major roles in CELL ADHESION; SIGNAL TRANSDUCTION; and regulation of angiogenesis. CD36 is a receptor for THROMBOSPONDINS and can act as a scavenger receptor that recognizes and transports oxidized LIPOPROTEINS and FATTY ACIDS.

Specific regional transcription of apolipoprotein E in human brain neurons. (1/5038)

In central nervous system injury and disease, apolipoprotein E (APOE, gene; apoE, protein) might be involved in neuronal injury and death indirectly through extracellular effects and/or more directly through intracellular effects on neuronal metabolism. Although intracellular effects could clearly be mediated by neuronal uptake of extracellular apoE, recent experiments in injury models in normal rodents and in mice transgenic for the human APOE gene suggest the additional possibility of intraneuronal synthesis. To examine whether APOE might be synthesized by human neurons, we performed in situ hybridization on paraffin-embedded and frozen brain sections from three nondemented controls and five Alzheimer's disease (AD) patients using digoxigenin-labeled antisense and sense cRNA probes to human APOE. Using the antisense APOE probes, we found the expected strong hybridization signal in glial cells as well as a generally fainter signal in selected neurons in cerebral cortex and hippocampus. In hippocampus, many APOE mRNA-containing neurons were observed in sectors CA1 to CA4 and the granule cell layer of the dentate gyrus. In these regions, APOE mRNA containing neurons could be observed adjacent to nonhybridizing neurons of the same cell class. APOE mRNA transcription in neurons is regionally specific. In cerebellar cortex, APOE mRNA was seen only in Bergmann glial cells and scattered astrocytes but not in Purkinje cells or granule cell neurons. ApoE immunocytochemical localization in semi-adjacent sections supported the selectivity of APOE transcription. These results demonstrate the expected result that APOE mRNA is transcribed and expressed in glial cells in human brain. The important new finding is that APOE mRNA is also transcribed and expressed in many neurons in frontal cortex and human hippocampus but not in neurons of cerebellar cortex from the same brains. This regionally specific human APOE gene expression suggests that synthesis of apoE might play a role in regional vulnerability of neurons in AD. These results also provide a direct anatomical context for hypotheses proposing a role for apoE isoforms on neuronal cytoskeletal stability and metabolism.  (+info)

Transcription factor AP-2 activity is modulated by protein kinase A-mediated phosphorylation. (2/5038)

We recently reported that APOE promoter activity is stimulated by cAMP, this effect being mediated by factor AP-2 [Garcia et al. (1996) J. Neurosci. 16, 7550-7556]. Here, we study whether cAMP-induced phosphorylation modulates the activity of AP-2. Recombinant AP-2 was phosphorylated in vitro by protein kinase A (PKA) at Ser239. Mutation of Ser239 to Ala abolished in vitro phosphorylation of AP-2 by PKA, but not the DNA binding activity of AP-2. Cotransfection studies showed that PKA stimulated the effect of AP-2 on the APOE promoter, but not that of the S239A mutant. Therefore, cAMP may modulate AP-2 activity by PKA-induced phosphorylation of this factor.  (+info)

Age of onset in Huntington disease: sex specific influence of apolipoprotein E genotype and normal CAG repeat length. (3/5038)

Age of onset (AO) of Huntington disease (HD) is known to be correlated with the length of an expanded CAG repeat in the HD gene. Apolipoprotein E (APOE) genotype, in turn, is known to influence AO in Alzheimer disease, rendering the APOE gene a likely candidate to affect AO in other neurological diseases too. We therefore determined APOE genotype and normal CAG repeat length in the HD gene for 138 HD patients who were previously analysed with respect to CAG repeat length. Genotyping for APOE was performed blind to clinical information. In addition to highlighting the effect of the normal repeat length upon AO in maternally inherited HD and in male patients, we show that the APOE epsilon2epsilon3 genotype is associated with significantly earlier AO in males than in females. Such a sex difference in AO was not apparent for any of the other APOE genotypes. Our findings suggest that subtle differences in the course of the neurodegeneration in HD may allow interacting genes to exert gender specific effects upon AO.  (+info)

Competition of Abeta amyloid peptide and apolipoprotein E for receptor-mediated endocytosis. (4/5038)

The genetic polymorphism of apolipoprotein E (apoE) is associated with the age of onset and relative risk of Alzheimer's disease (AD). In contrast to apoE3, the wild type allele, apoE4 confers an increased risk of late-onset AD. We demonstrate that the beta-amyloid peptide isoforms Abeta (1-28), Abeta (1-40), and Abeta (1-43) compete for the cellular metabolism of apoE3 and apoE4 containing beta-very low density lipoproteins. An antibody raised against Abeta (1-28) cross-reacted with recombinant apoE. Epitope mapping revealed positive amino acid clusters as common epitopes of Abeta (13 through 17; HHQKL) and apoE (residues 144 through 148; LRKRL), both regions known to be heparin binding domains. Abeta in which amino acids 13 through 17 (HHQKL) were replaced by glycine (GGQGL) failed to compete with the cellular uptake of apoE enriched betaVLDL. These observations indicate that Abeta and apoE are taken up into cells by a common pathway involving heparan sulfate proteoglycans.  (+info)

Mass spectral study of polymorphism of the apolipoproteins of very low density lipoprotein. (5/5038)

New isoforms of apolipoprotein (apo)C-I and apoC-III have been detected in delipidated fractions from very low density lipoprotein (VLDL) using matrix-assisted laser desorption (MALDI) and electrospray ionization (ESI) mass spectrometry (MS). The cleavage sites of truncated apoC-III isoforms have also been identified. The VLDL fractions were isolated by fixed-angle single-spin ultracentrifugation using a self-generating sucrose density gradient and delipidated using a newly developed C18 solid phase extraction protocol. Fifteen apoC isoforms and apoE were identified in the MALDI spectra and the existence of the more abundant species was verified by ESI-MS. The relative intensities of the apoCs are closely correlated in three normolipidemic subjects. A fourth subject with type V hyperlipidemia exhibited an elevated apoC-III level and a suppressed level of the newly discovered truncated apoC-I isoform. ApoC-II was found to be particularly sensitive to in vitro oxidation. The dynamic range and specificity of the MALDI assay shows that the complete apoC isoform profile and apoE phenotype can be obtained in a single measurement from the delipidated VLDL fraction.  (+info)

beta-amyloid load is not influenced by the severity of cardiovascular disease in aged and demented patients. (6/5038)

BACKGROUND AND PURPOSE: This study was conducted to analyze the association between reported risk factors for Alzheimer's disease, apolipoprotein E epsilon4 allele, and cardiovascular disease and neuropathological changes essential for the diagnosis of Alzheimer's disease. METHODS: Our data are based on clinical and postmortem evaluations of a cohort of nondemented (n=118) and demented (n=107) individuals. A cardiovascular index was calculated at autopsy to estimate the extent of cardiovascular disease. Neuropathological lesions such as senile/neuritic plaques, neurofibrillary tangles, beta-amyloid load, cerebral amyloid angiopathy, and the load of paired helical filaments were determined. RESULTS: The aforementioned neuropathological lesions did not show any positive significant correlation with cardiovascular index. In contrast, the extent of Alzheimer's lesions was significantly higher in those nondemented and demented patients carrying the apolipoprotein E epsilon4 allele than in those without this allele. CONCLUSIONS: Our results demonstrate that the apolipoprotein E epsilon4 allele, but not cardiovascular disease, indeed influences the extent of Alzheimer's lesions seen in the brain tissue of demented patients as well as asymptomatic controls.  (+info)

Apo E phenotype and changes in serum lipids in adult patients during growth hormone replacement. (7/5038)

OBJECTIVE: To determine whether apo E phenotype influences changes in lipid profiles induced by growth hormone replacement in growth hormone (GH)-deficient adults. DESIGNS: Patients were treated for 6 months with recombinant human GH (hGH), given in a dose of 0.125 U/kg per week for 4 weeks followed by 0.25 U/kg per week thereafter. The effects on serum lipids and the influence of apo E phenotype were examined. METHODS: Thirty patients (aged 35.1+/-11.8 years: mean +/- S.D.) with adult growth hormone deficiency with included in the study. Fasting serum samples were analysed for apo E phenotype total cholesterol, high-density lipoprotein (HDL)-cholesterol, triglycerides, lipoprotein (a) (Lp(a)) and IGF-I. Low-density lipoprotein (LDL)-cholesterol was calculated using the Friedwald formula. RESULTS: Six months of replacement treatment with hGH resulted in a reduction in HDL-cholesterol from 0.90+/-0.10 to 0.68+/-0.08 mmol/l (P<0.01), and a small, non-significant reduction in total cholesterol from 6.14+/-0.40 to 5.99+/-0.35 mmol/l (P = 0.06). There was no significant change in the other lipid parameters. The decrease in HDL-cholesterol concentration was greater in patients carrying the apo E2 allele (0.40+/-0.07 mmol/l, P<0.05) than in patients homozygous for the apo E3 allele (0.23+/-0.04 mmol/l) and patients carrying the apo E4 allele (0.15+/-0.36 mmol/l). Patients with the apo E4 allele had lower baseline cholesterol concentrations than patients lacking the apo E4 allele, and this persisted after treatment with hGH (P<0.05). CONCLUSIONS: Apo E phenotype may be a determining factor in the response of HDL-cholesterol to hGH in GH-deficient adults.  (+info)

Iron-deficient diet reduces atherosclerotic lesions in apoE-deficient mice. (8/5038)

BACKGROUND: Iron deposition is evident in human atherosclerotic lesions, suggesting that iron may play a role in the development of atherosclerosis. To test this idea, the correlation between the extent of iron deposition and the severity of atherosclerosis in apolipoprotein E (apoE)-deficient mice was investigated. Furthermore, the effect of a low-iron diet on the progression of atherosclerotic lesions in these animals was evaluated. METHODS AND RESULTS: Iron deposition in tissues of apoE-deficient mice was examined by Perls' staining method. The results clearly demonstrated that iron deposits are present in atherosclerotic lesions and tissue sections of heart and liver in an age-dependent manner. When the young mice received a low-iron diet for 3 months, the hematocrit, serum iron, hemoglobin, and cholesterol concentrations were not significantly altered compared with those of littermates placed on a chow diet. However, the serum ferritin level of animals in the iron-restricted group was 27% to 30% lower than that of the control group in either sex. Furthermore, the lipoproteins isolated from the iron-restricted group exhibited greater resistance to copper-induced oxidation. Histological examination revealed that atherosclerotic lesions developed in mice fed a low-iron diet were significantly smaller than those found in control littermates. Likewise, the iron deposition as well as tissue iron content was much less in aortic tissues of the iron-restricted animals. Circulating autoantibodies to oxidized LDL and immunostains for epitopes of malondialdehyde-modified LDL detected on lesions were also significantly lower in mice fed a low-iron diet. CONCLUSIONS: Iron deposition is closely associated with the progression of atherosclerosis in apoE-deficient mice. Restriction in dietary iron intake leads to significant inhibition of lesion formation in these animals. These results suggest that the beneficial effect of a low-iron diet may be mediated, at least in part, by the reduction of iron deposition as well as LDL oxidation in vascular lesions.  (+info)

AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesDisciplines and OccupationsTechnology, Industry, AgricultureInformation Science
Apolipoproteins EApolipoproteins CApolipoproteinsApolipoprotein C-IIIApolipoprotein E3Apolipoproteins ALipoproteinsApolipoproteins BApolipoprotein A-IApolipoprotein A-IIApolipoprotein C-IILipoproteins, HDLApolipoproteins DApolipoprotein C-ICholesterolLipoproteins, VLDLTriglyceridesLipidsApolipoprotein B-100Apolipoprotein B-48Cholesterol, HDLLipoproteins, HDL3Tangier DiseasePhosphatidylcholine-Sterol O-AcyltransferaseLipoproteins, LDLNephelometry and TurbidimetryATP Binding Cassette Transporter 1Cholesterol EstersIsoelectric FocusingReceptors, LipoproteinLipid MetabolismChylomicronsCholesterol, LDLPhospholipidsUltracentrifugationHypolipoproteinemiasLipoproteins, HDL2Lipoprotein(a)LymphElectrophoresis, Polyacrylamide GelApoproteinsHyperlipidemiasLiverImmunodiffusionLipoprotein LipaseTrioleinHyperlipoproteinemia Type IVPhosphatidylcholinesKineticsATP-Binding Cassette TransportersHyperlipoproteinemiasChemistry, ClinicalCholesterol, VLDLHypertriglyceridemiaCholesterol Ester Transfer ProteinsLipoproteins, IDLReference ValuesScavenger Receptors, Class BFreeze DryingEthinyl EstradiolParticle SizeImmunoassaySerum Amyloid A ProteinDietary FatsMicroscopy, ElectronImmunoelectrophoresisHyperlipoproteinemia Type VAbetalipoproteinemiaDimyristoylphosphatidylcholineReceptors, ScavengerAmino Acid SequenceOleic AcidChromatography, GelMolecular WeightArteriosclerosisBiological TransportLipolysisSterol O-AcyltransferaseRats, Inbred StrainsCallitrichinaeHigh-Density Lipoproteins, Pre-betaLipaseLiposomesReceptors, LDLOleic AcidsCarrier ProteinsMolecular Sequence DataLecithin Acyltransferase DeficiencyHyperlipidemia, Familial CombinedProtein BindingAntigens, CD36

*Apolipoprotein C2

... or apolipoprotein C-II is a protein that in humans is encoded by the APOC2 gene. secreted in plasma where it ... "A nonsense mutation in the apolipoprotein C-IIPadova gene in a patient with apolipoprotein C-II deficiency". J. Clin. Invest. ... Familial apolipoprotein CII deficiency associated with premature vascular disease". J. Clin. Invest. 80 (6): 1597-606. doi: ... "Structure of apolipoprotein C-IIToronto, a nonfunctional human apolipoprotein". Proc. Natl. Acad. Sci. U.S.A. 84 (1): 270-3. ...

*Lipid

In animals, when there is an oversupply of dietary carbohydrate, the excess carbohydrate is converted to triglycerides. This involves the synthesis of fatty acids from acetyl-CoA and the esterification of fatty acids in the production of triglycerides, a process called lipogenesis.[87] Fatty acids are made by fatty acid synthases that polymerize and then reduce acetyl-CoA units. The acyl chains in the fatty acids are extended by a cycle of reactions that add the acetyl group, reduce it to an alcohol, dehydrate it to an alkene group and then reduce it again to an alkane group. The enzymes of fatty acid biosynthesis are divided into two groups, in animals and fungi all these fatty acid synthase reactions are carried out by a single multifunctional protein,[88] while in plant plastids and bacteria separate enzymes perform each step in the pathway.[89][90] The fatty acids may be subsequently converted to triglycerides that are packaged in lipoproteins and secreted from the liver. The synthesis of ...

*Familial hypercholesterolemia

Apolipoprotein BEdit. Apolipoprotein B, in its ApoB100 form, is the main apolipoprotein, or protein part of the lipoprotein ... Class III: LDLR does not properly bind LDL on the cell surface because of a defect in either apolipoprotein B100 (R3500Q) or in ... LDL cholesterol normally circulates in the body for 2.5 days, and subsequently the apolipoprotein B portion of LDL cholesterol ... or apolipoprotein B (ApoB), which is the part of LDL that binds with the receptor; mutations in other genes are rare.[1] People ...

*Category:Blood proteins

Text is available under the Creative Commons Attribution-ShareAlike License; additional terms may apply. By using this site, you agree to the Terms of Use and Privacy Policy. Wikipedia® is a registered trademark of the Wikimedia Foundation, Inc., a non-profit organization ...

*Genetic testing

Apolipoprotein E-associated. Elevation of both serum cholesterol and triglycerides; accelerated atherosclerosis, coronary heart ...

*Lipocalin

... apolipoprotein D; beta-lactoglobulin; complement component C8 gamma chain; crustacyanin; epididymal-retinoic acid binding ...

*ApoA-1 Milano

Apolipoprotein A-1 Milano (also ETC-216, now MDCO-216) is a naturally occurring mutated variant of the apolipoprotein A1 ... Weisgraber KH, Rall SC, Bersot TP, Mahley RW, Franceschini G, Sirtori CR (25 February 1983). "Apolipoprotein A-IMilano. ...

*APOA2

Apolipoprotein A-II is a protein that in humans is encoded by the APOA2 gene. This gene encodes apolipoprotein (apo-) A-II, ... "Entrez Gene: APOA2 apolipoprotein A-II". Pussinen PJ, Jauhiainen M, Metso J, Pyle LE, Marcel YL, Fidge NH, Ehnholm C (Jan 1998 ... Brewer HB, Lux SE, Ronan R, John KM (May 1972). "Amino acid sequence of human apoLp-Gln-II (apoA-II), an apolipoprotein ... The protein is found in plasma as a monomer, homodimer, or heterodimer with apolipoprotein D. Defects in this gene may result ...

*Low-density lipoprotein receptor-related protein 8

Apolipoprotein E (ApoE) plays an important role in phospholipid and cholesterol homeostasis. After binding ApoER2, ApoE is ... Riddell DR, Sun XM, Stannard AK, Soutar AK, Owen JS (2001). "Localization of apolipoprotein E receptor 2 to caveolae in the ... Herz J (June 2009). "Apolipoprotein E receptors in the nervous system". Curr. Opin. Lipidol. 20 (3): 190-6. doi:10.1097/MOL. ... Low-density lipoprotein receptor-related protein 8 (LRP8), also known as apolipoprotein E receptor 2 (ApoER2), is a protein ...

*APOM

Apolipoprotein M is a protein that in humans is encoded by the APOM gene. The protein encoded by this gene is an apolipoprotein ... "Entrez Gene: APOM apolipoprotein M". Albertella MR, Jones H, Thomson W, et al. (1997). "Localization of eight additional genes ... 2004). "Regulation of apolipoprotein M gene expression by MODY3 gene hepatocyte nuclear factor-1alpha: haploinsufficiency is ... 2005). "Leptin inhibits apolipoprotein M transcription and secretion in human hepatoma cell line, HepG2 cells". Biochim. ...

*APOL3

Apolipoprotein L3 is a protein that in humans is encoded by the APOL3 gene. This gene is a member of the apolipoprotein L gene ... "Entrez Gene: APOL3 apolipoprotein L, 3". Human APOL3 genome location and APOL3 gene details page in the UCSC Genome Browser. ... 2001). "Apolipoprotein L gene family: tissue-specific expression, splicing, promoter regions; discovery of a new gene". J. ... Monajemi H, Fontijn RD, Pannekoek H, Horrevoets AJ (2002). "The apolipoprotein L gene cluster has emerged recently in evolution ...

*Gladstone Institutes

Alzheimer's disease and apolipoprotein E (apoE). Uncovered the molecular pathways that link apoE and Alzheimer's disease, and ...

*APOL2

Apolipoprotein L2 is a protein that in humans is encoded by the APOL2 gene. This gene is a member of the apolipoprotein L gene ... "Entrez Gene: APOL2 apolipoprotein L, 2". Human APOL2 genome location and APOL2 gene details page in the UCSC Genome Browser. ... McGhee KA, Morris DW, Schwaiger S (2005). "Investigation of the apolipoprotein-L (APOL) gene family and schizophrenia using a ... Monajemi H, Fontijn RD, Pannekoek H, Horrevoets AJ (2002). "The apolipoprotein L gene cluster has emerged recently in evolution ...

*APOL6

Apolipoprotein L6 is a protein that in humans is encoded by the APOL6 gene. This gene is a member of the apolipoprotein L gene ... "Entrez Gene: APOL6 apolipoprotein L, 6". Human APOL6 genome location and APOL6 gene details page in the UCSC Genome Browser. ... Liu Z, Lu H, Jiang Z, Pastuszyn A, Hu CA (Jan 2005). "Apolipoprotein l6, a novel proapoptotic Bcl-2 homology 3-only protein, ... "The human apolipoprotein L gene cluster: identification, classification, and sites of distribution". Genomics. 74 (1): 71-8. ...

*Bleomycin hydrolase

2003). "[Apolipoprotein E and bleomycin hydrolase. Polymorphisms: association with neurodegenerative diseases]". Ann. Biol. ...

*Farnesoid X receptor

"Farnesoid X receptor agonists suppress hepatic apolipoprotein CIII expression". Gastroenterology. 125 (2): 544-55. doi:10.1016/ ...

*APOA4

Karathanasis SK (1985). "Apolipoprotein multigene family: tandem organization of human apolipoprotein AI, CIII, and AIV genes ... "Genetic polymorphism of human plasma apolipoprotein A-IV is due to nucleotide substitutions in the apolipoprotein A-IV gene". J ... Apolipoprotein A-IV (also known as apoA-IV, apoAIV, or apoA4) is plasma protein that is the product of the human gene APOA4. ... "Entrez Gene: APOA4 apolipoprotein A-IV". Luo CC, Li WH, Moore MN, Chan L (February 1986). "Structure and evolution of the ...

*High-density lipoprotein

Its most abundant apolipoproteins are apo A-I and apo A-II. A rare genetic variant, ApoA-1 Milano, has been documented to be ... In the stress response, serum amyloid A, which is one of the acute-phase proteins and an apolipoprotein, is under the ... Sacks FM, Zheng C, Cohn JS (2011). "Complexities of plasma apolipoprotein C-III metabolism". Journal of Lipid Research. 52 (6 ... HDL lipoprotein particles that bear apolipoprotein C3 are associated with increased, rather than decreased, risk for coronary ...

*APOBEC4

"Entrez Gene: apolipoprotein B mRNA editing enzyme". Marino D, Perković M, Hain A, Jaguva Vasudevan AA, Hofmann H, Hanschmann KM ... C->U-editing enzyme APOBEC-4, also known as Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 4, is a protein ...

*Hepatocyte nuclear factor 4 alpha

Zannis VI, Kan HY, Kritis A, Zanni E, Kardassis D (Mar 2001). "Transcriptional regulation of the human apolipoprotein genes". ... Ginsburg GS, Ozer J, Karathanasis SK (Jul 1995). "Intestinal apolipoprotein AI gene transcription is regulated by multiple ... "CREB-binding protein is a transcriptional coactivator for hepatocyte nuclear factor-4 and enhances apolipoprotein gene ...

*APOLD1

Apolipoprotein L domain containing 1". Retrieved 2012-11-02. APOLD1 apolipoprotein L domain containing 1 [ Homo sapiens (human ... Apolipoprotein L domain containing 1 is a protein in humans that is encoded by the APOLD1 gene. It is located on Chromosome 12 ...

*DAB1

1999) showed that 2 cell surface receptors, very low density lipoprotein receptor (VLDLR; 192977) and apolipoprotein E receptor ... "Functional dissection of Reelin signaling by site-directed disruption of Disabled-1 adaptor binding to apolipoprotein E ...

*Harold Smith (scientist)

L Chan (22 May 1994). "Apolipoprotein B Messenger RNA editing: An Update". Departments of Cell Biology and Medicine, Baylor ...

*Mothers against decapentaplegic homolog 2

Zannis VI, Kan HY, Kritis A, Zanni E, Kardassis D (March 2001). "Transcriptional regulation of the human apolipoprotein genes ...

*Alcohol-related dementia

The presence of the Apolipoprotein c4 allele. If the symptoms of alcohol dementia are caught early enough, the effects may be ...
Overexpression of perilipin1 protects against atheroma progression in apolipoprotein E knockout mice : HUSCAP  Overexpression of perilipin1 protects against atheroma progression in apolipoprotein E knockout mice : HUSCAP
Background and aims: Perilipin1 (PLIN1), a lipid droplet-associated protein, plays an important role in the regulation of lipolysis and lipid storage in adipocytes. PLIN1 has recently been reported to be expressed in macrophages within atheroma plaques, suggesting PLIN1 may play a role in the accumulation of lipids at the arterial wall and in the development of atherosclerosis. To clarify the role of PLIN1 in the pathophysiology of atherosclerosis, we assessed the progression of atherosclerosis in PLIN1 transgenic mice (Plin1Tg). Methods: Plin1Tg were crossed with apolipoprotein E knockout mice (ApoeKO). C57BL/6J mice, ApoeKO and Plin1Tg/ApoeKO received a normal chow diet for 20 weeks. Body weight, gonadal fat mass and plasma lipid concentrations were measured. Aortas were collected for quantification of atheroma lesions and histological analysis by Oil Red O staining. Results: Body weight, gonadal adipose mass and plasma triglyceride concentrations were not significantly different among the ...
https://eprints.lib.hokudai.ac.jp/dspace/handle/2115/68843
Apolipoprotein E genotype in Spanish patients of Alzheimers or Parkinsons disease. - Semantic Scholar  Apolipoprotein E genotype in Spanish patients of Alzheimer's or Parkinson's disease. - Semantic Scholar
Blood donors of the Madrid area show a 6% frequency of apolipoprotein E genotype carrying allele epsilon 4. This frequency is smaller than other populations of Caucasian origin. This proportion decreases to 4% in a selected sample of healthy individuals of ages | 60 years. The frequency (34%) of the allele epsilon 4 was significantly increased in patients of late onset Alzheimers disease, similarly to other populations. An earlier age of onset of the dementia is observed in the patients of late-onset Alzheimers disease carrying the allele epsilon 4. No increased frequency in allele epsilon 4 frequency was found in patients of early-onset Alzheimers disease. Patients of Parkinsons disease do not show any differences in the frequency of the alleles of apolipoprotein E when compared with healthy individuals.
https://www.semanticscholar.org/paper/Apolipoprotein-E-genotype-in-Spanish-patients-of-A-Ibarreta-G%C3%B3mez-Isla/b8d17bf9babd33c792d5eb05443d721a3a9b4c5a
Expression of the human apolipoprotein E gene suppresses steroidogenesis in mouse Y1 adrenal cells. | PNAS  Expression of the human apolipoprotein E gene suppresses steroidogenesis in mouse Y1 adrenal cells. | PNAS
The lipid transport protein, apolipoprotein E (apoE), is expressed in many peripheral tissues in vivo including the adrenal gland and testes. To investigate the role of apoE in adrenal cholesterol homeostasis, we have expressed a human apoE genomic clone in the Y1 mouse adrenocortical cell line. Y1 cells do not express endogenous apoE mRNA or protein. Expression of apoE in Y1 cells resulted in a dramatic decrease in basal steroidogenesis; secretion of fluorogenic steroid was reduced 7- to greater than 100-fold relative to Y1 parent cells. Addition of 5-cholesten-3 beta,25-diol failed to overcome the suppression of steroidogenesis in these cells. Cholesterol esterification under basal conditions, as measured by the production of cholesteryl [14C]oleate, was similar in the Y1 parent and the apoE-transfected cell lines. Upon incubation with adrenocorticotropin or dibutyryl cAMP, production of cholesteryl [14C]oleate decreased 5-fold in the Y1 parent cells but was unchanged in the apoE-transfected ...
https://www.pnas.org/content/88/6/2375
Regulation of Endogenous Apolipoprotein E Secretion by Macrophages | Arteriosclerosis, Thrombosis, and Vascular Biology  Regulation of Endogenous Apolipoprotein E Secretion by Macrophages | Arteriosclerosis, Thrombosis, and Vascular Biology
Recent studies in other systems have demonstrated that constitutive protein secretion is regulated, and involves kinases, phosphatases, receptors, and typically, the microtubule network.76,83,84 In view of previous studies indicating that apoE secretion could be stimulated by apoA-I and by HDL,17,19,38,47 we hypothesized that even basal apoE secretion must be under some form of regulation. We showed that disruption of microtubules inhibited basal apoE secretion, whereas disruption of the actin skeleton had no effect. Microscopy studies supported this by showing alignment of apoE-containing vesicles along the microtubules but not the actin cytoskeleton in RAW macrophages.49. Protein kinase A (PKA) regulates traffic of several proteins at different steps in the constitutive secretory pathway,85 and a range of PKA inhibitors decreased secretion of apoE.49 Live cell imaging of apoE-GFP-transfected RAW macrophages indicated that PKA is required for the movement of apoE-containing vesicles. ...
http://atvb.ahajournals.org/content/28/6/1060
北京大学医学部机构知识库(IR@PKUHSC): Beijing ambient particle exposure accelerates atherosclerosis in ApoE knockout mice  北京大学医学部机构知识库([email protected]): Beijing ambient particle exposure accelerates atherosclerosis in ApoE knockout mice
Background: Air pollution is associated with significant adverse health effects including increased cardiovascular morbidity and mortality. However research on the cardiovascular effect of "real-world" exposure to ambient particulate matter (PM) in susceptible animal model is very limited. In this study, we aimed to investigate the association between Beijing ambient particle exposure and the atherosclerosis development in the apolipoprotein E knockout mice (ApoE-/-mice).. Methods: Two parallel exposure chambers were used for whole body exposure among ApoE knockout mice. One of the chambers was supplied with untreated ambient air (PM group) and the other chamber was treated with ambient air filtered by high-efficiency particulate air (HEPA) filter (FA group). Twenty mice were divided into two groups and exposed to ambient PM (n = 10 for PM group) or filtered air(n = 10 for FA group) for two months from January 18th to March 18th, 2010. During the exposure, the mass concentrations of PM2.5 and ...
http://ir.bjmu.edu.cn/handle/400002259/65374
The effect of APOE genotype on brain levels of oxysterols in young and old human APOE ε2,ε3 and ε4 knock-in mice | ScholarBank...  The effect of APOE genotype on brain levels of oxysterols in young and old human APOE ε2,ε3 and ε4 knock-in mice | ScholarBank...
Despite apolipoprotein Es important role in cholesterol transport and metabolism in the brain as well as its influence on Alzheimers disease, the impact of the human APOE genotype on cholesterol metabolism in brain has not been fully examined. This study was carried out to investigate APOE genotype effects on oxysterols measured. In this study the measurement of cholesterol and several oxysterols in the brains of human APOE ε2, ε3 and ε4 knock-in mice at 8 weeks and 1 year of age using gas chromatography mass spectrometry (GC-MS) demonstrated no APOE genotype or age effect on total brain cholesterol and the oxysterol 24-hydroxycholesterol. The level of 27-hydroxycholesterol was elevated in 1 year old animals for all APOE genotypes. Interestingly, lathosterol an indicator of cholesterol synthesis was significantly reduced in the 1 year old animals for all APOE genotypes. APOE ε4 expressing mice exhibited statistically lower levels of lathosterol compared to APOE ε2 in both the young and ...
http://scholarbank.nus.edu.sg/handle/10635/28936
Frontiers | Renal Denervation Promotes Atherosclerosis in Hypertensive Apolipoprotein E-Deficient Mice Infused with Angiotensin...  Frontiers | Renal Denervation Promotes Atherosclerosis in Hypertensive Apolipoprotein E-Deficient Mice Infused with Angiotensin...
Objective: To determine the effect of renal denervation (RDN) on the severity of atherosclerosis and aortic aneurysm in hypertensive mice. Methods: Hypertension, atherosclerosis and aortic aneurysm were induced by subcutaneous infusion of angiotensin II (1 µg/kg/min) for 28 days in apolipoprotein E-deficient mice. RDN was conducted using combined surgical and local chemical denervation. The norepinephrine concentration in the kidney was measured by high-performance liquid chromatography. Blood pressure was measured by the tail-cuff method. Atherosclerosis was assessed by Sudan IV staining of the aortic arch. The aortic diameter was measured by the morphometric method. The mRNA expression of genes associated with atherosclerosis and aortic aneurysm were analyzed by quantitative PCR. Results: RDN decreased the median norepinephrine content in the kidney by 93.4% (n=5-7, P=0.003) five days after the procedure, indicating that the RDN procedure was successful. RDN decreased systolic blood pressure in
https://www.frontiersin.org/articles/10.3389/fphys.2017.00215/full
Investigation of sex-specific effects of apolipoprotein E on severity of EAE and MS | Journal of Neuroinflammation | Full Text  Investigation of sex-specific effects of apolipoprotein E on severity of EAE and MS | Journal of Neuroinflammation | Full Text
Despite pleiotropic immunomodulatory effects of apolipoprotein E (apoE) in vitro, its effects on the clinical course of experimental autoimmune encephalomyelitis (EAE) and multiple sclerosis (MS) are still controversial. As sex hormones modify immunomodulatory apoE functions, they may explain contentious findings. This study aimed to investigate sex-specific effects of apoE on disease course of EAE and MS. MOG35-55 induced EAE in female and male apoE-deficient mice was assessed clinically and histopathologically. apoE expression was investigated by qPCR. The association of the MS severity score (MSSS) and APOE rs429358 and rs7412 was assessed across 3237 MS patients using linear regression analyses. EAE disease course was slightly attenuated in male apoE-deficient (apoE −/− ) mice compared to wildtype mice (cumulative median score: apoE −/− = 2 [IQR 0.0-4.5];
https://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-015-0429-y
Anti-apoE immunotherapy inhibits amyloid accumulation in a transgenic mouse model of Aβ amyloidosis | Journal of Experimental...  Anti-apoE immunotherapy inhibits amyloid accumulation in a transgenic mouse model of Aβ amyloidosis | Journal of Experimental...
Given its ability to detect apoE in amyloid plaques (Fig. 1 F), we selected HJ6.3 antibody for anti-apoE immunization experiments. To determine whether anti-apoE antibody would have an antiamyloidogenic effect, we injected PBS or anti-apoE antibody (HJ6.3) weekly at 10 mg of antibody/kg of body weight per dose. 4-mo-old male APPswe/PS1ΔE9 mice were intraperitoneally injected for 14 wk. Brain tissues were processed for histochemical and biochemical analyses. Quantitative analyses of anti-Aβ immunostaining (Fig. 2, A and B) demonstrated that Aβ plaque load in the cortex (Fig. 2 C) and hippocampus (Fig. 2 D) was markedly decreased by HJ6.3 antibody treatment, compared with the PBS-treated control group. There was a strong 70-80% reduction in Aβ plaque load in the cortex (Fig. 2 C) and hippocampus (Fig. 2 D). HJ6.3 treatment also significantly decreased the number of plaques per area in the cortex (Fig. 2 E) and hippocampus (Fig. 2 F). To further characterize the structural nature of the ...
https://rupress.org/jem/article/209/12/2149/41241/Anti-apoE-immunotherapy-inhibits-amyloid
CXCL16/SR-PSOX is an interferon-gamma-regulated chemokine and scavenger receptor expressed in atherosclerotic lesions  CXCL16/SR-PSOX is an interferon-gamma-regulated chemokine and scavenger receptor expressed in atherosclerotic lesions
article{a4a89a77-6245-40ad-adfc-12ba8e92c5b8, abstract = {OBJECTIVE: Atherosclerosis is an inflammatory disease. Several chemokines are important for monocyte/macrophage and T-cell recruitment to the lesion. CXCL16 is a recently discovered chemokine that is expressed in soluble and transmembrane forms, ligates CXCR6 chemokine receptor, and guides migration of activated Th1 and Tc1 cells. It is identical to scavenger receptor SR-PSOX, which mediates uptake of oxidized low-density lipoprotein. We investigated whether CXCL16 expression is controlled by interferon-gamma (IFN-gamma)-cytokine abundant in atherosclerotic lesions. METHODS AND RESULTS: CXCL16 and CXCR6 expression was identified by polymerase chain reaction and histochemistry in atherosclerotic lesions from humans and apolipoprotein-E-deficient mice. In vitro IFN-gamma induced CXCL16 in human monocytic THP-1 cells and primary human monocytes, which led to increased uptake of oxidized low-density lipoprotein in THP-1 cells, which could be ...
https://lup.lub.lu.se/search/publication/1129700
Natural History of Amyloid Deposition in Adults With Down Syndrome - Full Text View - ClinicalTrials.gov  Natural History of Amyloid Deposition in Adults With Down Syndrome - Full Text View - ClinicalTrials.gov
Specific Aim 1: To assess and compare amyloid deposition (with PiB PET) in non-demented/functionally stable adults with DS across three age cohorts (30-39, 40-49, and ,50 years of age).. Primary Hypothesis 1: At initial assessment, there will be a significantly higher prevalence of amyloid-positive (PiB+) subjects in each succeeding age cohort.. In addition, we will test the following secondary hypothesis:. Secondary Aim 1: To compare the presence or absence of the apolipoprotein-E4 allele to the retention of PiB in various brain areas of the DS subjects.. Secondary Hypothesis 1: At baseline, subjects who carry at least one Apolipoprotein-E4 (ApoE4) allele will show a higher prevalence of being PiB+. ...
https://clinicaltrials.gov/ct2/show/NCT01303133
Cytokine Therapy with IL-2/anti-IL-2mAb Complexes Expands CD4+CD25+Foxp3+ Regulatory T Cells and Attenuates Development and of...  Cytokine Therapy with IL-2/anti-IL-2mAb Complexes Expands CD4+CD25+Foxp3+ Regulatory T Cells and Attenuates Development and of...
Background-CD4+CD25+Foxp3+ regulatory T cells (Tregs) attenuate atherosclerosis but their therapeutic application by adoptive transfer is limited by the need for their expansion in vitro and limited purity. Recently, an IL-2/anti-IL-2 neutralizing mAb (IL-2/anti-IL-2 mAb) complex has been shown to expand these Tregs. We examined the capacity of a modified IL-2/anti-IL-2 mAb treatment to expand Tregs and inhibit both the progression and development of developed atherosclerosis. Methods and Results-Six-week old apolipoprotein-E-deficient mice fed a high fat diet for 8 weeks were administered IL-2/anti-IL-2 mAb commencing 2 weeks after starting the diet. Tregs in the spleen, lymph node and liver were selectively expanded without affecting CD4+, CD8+ or NK cells. Tregs were increased in lesions and lesion size reduced. CD4+ T-cells, macrophages, mature dendritic cells, PCNA+ cells and MCP-1 and VCAM-1 were reduced. In anti-CD3 stimulated splenocytes, proliferation and secretion of Th1, Th2, Th17 ...
http://circ.ahajournals.org/content/early/2012/07/31/CIRCULATIONAHA.112.099044
Low-Cholesterol and High-Fat Diets Reduce Atherosclerotic Lesion Development in ApoE-Knockout Mice | Arteriosclerosis,...  Low-Cholesterol and High-Fat Diets Reduce Atherosclerotic Lesion Development in ApoE-Knockout Mice | Arteriosclerosis,...
Although dietary fat is considered to be one of the risk factors for cardiovascular diseases, it is not well understood whether a high fat content in diet has an effect on lipid metabolism and on atherosclerotic lesion development when the amount of cholesterol in the diet is low. To address this issue and to study possible mechanisms by which dietary fat regulates such parameters, we have conducted a dietary trial in which apoE-knockout mice were given 7 different diets for 10 weeks. We found that dietary fat supplement without addition of cholesterol does not increase lesion sizes either in males or females. On the contrary, palm and olive II oils significantly reduced lesion size but only in female mice. Furthermore, different types of fat have different effects, and even a particular oil from different cultivars has different effects, as in the case of olive oil I and II. Reduction in lesion size was independent of plasma cholesterol levels because no change in the latter was observed in any ...
http://atvb.ahajournals.org/content/19/10/2368
Apelin Is a Negative Regulator of Angiotensin II-Mediated Adverse Myocardial Remodeling and DysfunctionNovelty and Significance...  Apelin Is a Negative Regulator of Angiotensin II-Mediated Adverse Myocardial Remodeling and DysfunctionNovelty and Significance...
The apelin pathway has emerged as a critical regulator of cardiovascular homeostasis and disease. However, the exact role of pyr1-apelin-13 in angiotensin (Ang) II-mediated heart disease remains unclear. We used apelin-deficient (APLN−/y) and apolipoprotein E knockout mice to evaluate the regulatory roles of pyr1-apelin-13. The 1-year aged APLN−/y mice developed myocardial hypertrophy and dysfunction with reduced angiotensin-converting enzyme 2 levels. Ang II infusion (1.5 mg kg−1 d−1) for 4 weeks potentiated oxidative stress, pathological hypertrophy, and myocardial fibrosis in young APLN−/y hearts resulting in exacerbation of cardiac dysfunction. Importantly, daily administration of 100 μg/kg pyr1-apelin-13 resulted in upregulated angiotensin-converting enzyme 2 levels, decreased superoxide production and expression of hypertrophy- and fibrosis-related genes leading to attenuated myocardial hypertrophy, fibrosis, and dysfunction in the Ang II-infused apolipoprotein E knockout mice. ...
http://hyper.ahajournals.org/content/70/6/1165
Pioglitazone ameliorates glomerular NLRP3 inflammasome activation in apolipoprotein E knockout mice with diabetes mellitus  Pioglitazone ameliorates glomerular NLRP3 inflammasome activation in apolipoprotein E knockout mice with diabetes mellitus
by Yao Wang, Bo Yu, Li Wang, Ming Yang, Zhiyin Xia, Wei Wei, Fengyu Zhang, Xiaochen Yuan Objective The NLRP3 inflammasome plays an important role in the pathogenesis of inflammation in diabetic ...
https://www.bionity.com/en/publications/1103031/pioglitazone-ameliorates-glomerular-nlrp3-inflammasome-activation-in-apolipoprotein-e-knockout-mice-with-diabetes-mellitus.html
Transplantation of Bone Marrow-Derived Mononuclear Cells in Ischemic Apolipoprotein E-Knockout Mice Accelerates Atherosclerosis...  Transplantation of Bone Marrow-Derived Mononuclear Cells in Ischemic Apolipoprotein E-Knockout Mice Accelerates Atherosclerosis...
Therapeutic enhancement of neovascularization is one of the most important strategies needed to limit the complications of postischemic injury.2-4 However, many factors shown to play an important role in neovascularization, such as MCP-1 and VEGF, are potent proinflammatory mediators and promote the development and progression of atherosclerosis with an unstable potential in various experimental models,12,13 making their potential use in patients with advanced atherosclerosis unsuitable and even hazardous in acutely ill patients. The recent identification of a central role for BM-MNCs in tissue revascularization and preservation of function after ischemic injury has renewed the great hope for an efficient proangiogenic therapy with reduced side effects. As atherosclerotic plaque instability is the most important trigger of ischemic injury in patients who would benefit from proangiogenic therapies, these strategies should be evaluated for their potential to modulate atherosclerosis progression ...
http://circ.ahajournals.org/content/108/23/2839
Effect of Dietary Fat on LDL Size Influenced by Apolipoprotein E Genotype in Healthy Subjects - Lifestyle - LONGECITY  Effect of Dietary Fat on LDL Size Influenced by Apolipoprotein E Genotype in Healthy Subjects - Lifestyle - LONGECITY
Effect of Dietary Fat on LDL Size Influenced by Apolipoprotein E Genotype in Healthy Subjects - posted in Lifestyle: Any thoughts? I read this laymans article here which explains how smaller LDL particle size is a better predictor for increased risk of heart disease, and how high carbohydrate diets decrease the size of LDL particles.The paper below claims the opposite if you are ApoE3/4. Im ApoE3/4, and Ive discussed this topic on longecity before, so I guess Ill contin...
http://www.longecity.org/forum/topic/61878-effect-of-dietary-fat-on-ldl-size-influenced-by-apolipoprotein-e-genotype-in-healthy-subjects/
Plus it  Plus it
We report several new findings that are essential for understanding how apoE is regulated in the brain. The highest levels of apoE mRNA in both control and transgenic mice were found in astrocytes of the olfactory bulb and in Bergmann glia of the cerebellum. Analysis of multiple independent lines for each construct minimizes the possibility that differences in apoE mRNA transgene expression between constructs are because of integration artifacts or position effects. In the brain, apoE gene expression under the control of the ME.1 and ME.2 domains was detected only in astrocytes. Our data further suggest that astrocytes are responsible for a majority of apoE expression in the absence of inflammatory signals.. Astrocyte apoE expression was specified by distal regions located 3.3 kb and 15 kb downstream of the apoE gene. These distal sequences are 95% identical in nucleotide sequence, and they probably arose from the duplication event that yielded the two apoC-I genes (Fig. 1). In the absence of ...
http://www.jneurosci.org/content/21/3/812
Apolipoprotein E Genotype Does Not Affect the Changes in Serum Lipids by CL Meckes, NM Moyna et al.  "Apolipoprotein E Genotype Does Not Affect the Changes in Serum Lipids " by CL Meckes, NM Moyna et al.
Meckes, C., Moyna, N., Tsongalis, G., Miles, M. (2001). Apolipoprotein E Genotype Does Not Affect the Changes in Serum Lipids with Exercise Training. Circulation, 104(17), 343-343 ...
https://aquila.usm.edu/fac_pubs/3761/
anti-APOE antibody | anti-Mouse Apolipoprotein E (Apo E) Polyclonal Antibody-P02649.1  anti-APOE antibody | anti-Mouse Apolipoprotein E (Apo E) Polyclonal Antibody-P02649.1
Buy anti-APOE antibody, anti-Mouse Apolipoprotein E (Apo E) Polyclonal Antibody-P02649.1 (MBS315478) product datasheet at MyBioSource, Primary Antibodies. Application: DD, IEP, RID, Western Blot
https://www.mybiosource.com/prods/Antibody/Polyclonal/Apolipoprotein-E-Apo-E/APOE/datasheet.php?products_id=315478
Expression of Human Apolipoprotein E Downregulates Amyloid Precursor Protein-Induced Ischemic Susceptibility | Stroke  Expression of Human Apolipoprotein E Downregulates Amyloid Precursor Protein-Induced Ischemic Susceptibility | Stroke
Previous studies have demonstrated that endogenous mouse apoE is protective against transient focal and global brain ischemia and traumatic brain injury.34-36⇓⇓ Although human apoE isoforms markedly delay the appearance of Aβ deposition in APPV717F transgenic mice,14 apoE ultimately facilitates the neuritic degeneration associated with amyloid deposits and with conversion of Aβ into mature fibrillar amyloid,15 which is thought to be neurotoxic.37 In the present study, we show that neuronal overexpression of human APP751 at the level detected in early AD and Downs syndrome28 dramatically increases the susceptibility to ischemic brain damage in the absence of apoE. Moreover, expression of human apoE3 or apoE4 in astrocytes significantly reduces the neuronal vulnerability to ischemia in APP751 transgenic mice. These results indicate that even though apoE may be a contributory factor in Aβ-induced toxicity in AD, it has a beneficial role against APP751-induced ischemic vulnerability. ...
http://stroke.ahajournals.org/content/33/7/1905.long
JCI - Smooth muscle cell-specific fibronectin-EDA mediates phenotypic switching and neointimal hyperplasia  JCI - Smooth muscle cell-specific fibronectin-EDA mediates phenotypic switching and neointimal hyperplasia
Animals. Eight- to ten-week-old male and female WT, Fn-EDA-/-, Apoe-/-, Fn-EDA-/- Apoe-/-, TLR4-/- Apoe-/-, Fn-EDA-/- TLR4-/- Apoe-/-, and Fn-EDAfl/fl Apoe-/- mice on the C57BL/6J background, weighing around 22 ± 2 g, were used in this study. We have characterized and described these mice previously (40). Briefly, Fn-EDA-/- mice and Fn-EDAfl/fl mice (backcrossed ,15 times to C57BL/6J) were crossed to Apoe-/- mice (The Jackson Laboratory) to generate Fn-EDA-/- Apoe-/- mice and EDAfl/fl Apoe-/- mice, respectively. Apoe-/- mice were crossed to TLR4-/- mice to generate TLR4-/- Apoe-/- mice. Fn-EDA-/- Apoe-/- mice were crossed to TLR4-/- Apoe-/- mice to obtain Fn-EDA-/- TLR4-/- Apoe-/- mice. To generate SMC-specific Fn-EDA-deficient mice on an Apoe-deficient background, first SM22αCre+ mice were crossed with Apoe-/- mice to generate SM22αCre+ Apoe-/- mice. In the second step, Fn-EDAfl/fl Apoe-/- mice were crossed to SM22αCre+ Apoe-/- mice to generate Fn-EDAfl/fl SM22αCre+ Apoe-/- mice. To ...
https://cz7c.com.www.mobile.jci.org/articles/view/124708
The effects of APOE on the functional architecture of the resting brain. - Department of Psychiatry  The effects of APOE on the functional architecture of the resting brain. - Department of Psychiatry
There is a well-established association between APOE genotype and the risk of developing Alzheimers disease (AD). Relative to individuals with the common ε3/ε3 genotype, carriers of the ε4 allele are at increased risk of developing AD, while carriers of the ε2 allele appear to be protected against the disease. However, we recently reported that in a sample of cognitively healthy adults, both ε4 and ε2 carriers showed nearly identical changes in the pattern of fMRI activity during memory and non-memory tasks, relative to ε3 homozygotes. These findings suggest that the effects of APOE on brain function are not tightly linked to the effects of this gene on AD risk. Here we test the hypothesis that APOE has an intrinsic effect on the brains functional networks. Resting-state fMRI was used to compare the pattern of functional connectivity of a variety of resting-state networks between 77 cognitively healthy participants aged 32 to 55 with different APOE genotypes (23 ε2/ε3, 20 ε3/ε3, 26 ε3/ε4,
https://www.psych.ox.ac.uk/publications/177140
Specific penetration and accumulation of a homing peptide within atherosclerotic plaques of apolipoprotein E-deficient mice. -...  Specific penetration and accumulation of a homing peptide within atherosclerotic plaques of apolipoprotein E-deficient mice. -...
The ability to selectively deliver compounds into atherosclerotic plaques would greatly benefit the detection and treatment of atherosclerotic disease. We describe such a delivery system based on a 9-amino acid cyclic peptide, LyP-1. LyP-1 was originally identified as a tumor-homing peptide that specifically recognizes tumor cells, tumor lymphatics, and tumor-associated macrophages. As the receptor for LyP-1, p32, is expressed in atherosclerotic plaques, we tested the ability of LyP-1 to home to plaques. Fluorescein-labeled LyP-1 was intravenously injected into apolipoprotein E (ApoE)-null mice that had been maintained on a high-fat diet to induce atherosclerosis. LyP-1 accumulated in the plaque interior, predominantly in macrophages. More than 60% of cells released from plaques were positive for LyP-1 fluorescence. Another plaque-homing peptide, CREKA, which binds to fibrin-fibronectin clots and accumulates at the surface of plaques, yielded fewer positive cells. Tissues that did not contain plaque
https://www.semanticscholar.org/paper/Specific-penetration-and-accumulation-of-a-homing-Hamzah-Kotamraju/90b4a9985b3b139e9747b5f5e012e892f1ebb38c
A non-invasive, rapid screening method for Alzheimer... ( The apolipoprotein E gene ε4 all...)  A non-invasive, rapid screening method for Alzheimer... ( The apolipoprotein E gene ε4 all...)
...The apolipoprotein E gene ε4 allele is considered a negative fact......,A,non-invasive,,rapid,screening,method,for,Alzheimers,disease,biological,biology news articles,biology news today,latest biology news,current biology news,biology newsletters
http://www.bio-medicine.org/biology-news-1/A-non-invasive--rapid-screening-method-for-Alzheimers-disease-34764-1/
Red Wine administration to Apolipoprotein E-deficient Mice reduces their Macrophage-derived Extracellular Matrix Atherogenic...  Red Wine administration to Apolipoprotein E-deficient Mice reduces their Macrophage-derived Extracellular Matrix Atherogenic...
INTRODUCTION The development of atherosclerotic lesion is initiated with the accumulation of cholesterol in monocyte-derived macrophages (2,3) as well as with the retention of lipoproteins in the extracellular matrix of the subendothelial wall (22,30). Extracellular matrix (ECM) contains collagen and elastic fibers embedded in a viscoelastic gel consisting of proteoglycans (PGs), hyaluronan and glycoproteins (29). Arterial ECM contributes to the trapping of LDL and oxidized LDL (Ox-LDL) in the arterial wall, a phenomenon called lipoprotein retention (7, 18, 31). Specifically, the PGs from the ECM were shown to be responsible for the entrapment of LDL and Ox-LDL in the arterial wall (19, 27). Moreover, we have shown that subsequent to their binding to the matrix, LDL and Ox-LDL are taken up by macrophages (20). ECM can be produced in vitro by arterial cells, including endothelial cells, smooth muscle cells and also by macrophages (19). The amount and composition of ECM produced by all major ...
http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602004000200010&lng=es&nrm=iso
Cathepsin G deficiency decreases complexity of atherosclerotic lesions in apolipoprotein E-deficient mice. | Sigma-Aldrich  Cathepsin G deficiency decreases complexity of atherosclerotic lesions in apolipoprotein E-deficient mice. | Sigma-Aldrich
Sigma-Aldrich offers abstracts and full-text articles by [Naimeh Rafatian, Denuja Karunakaran, Katey J Rayner, Frans H H Leenen, Ross W Milne, Stewart C Whitman].
https://www.sigmaaldrich.com/catalog/papers/23934850
Last reviewed 26 Oct 2016  Last reviewed 26 Oct 2016
Gupta, V., Wilson, A., Burnham, S., Hone, E., Pedrini, S., Laws, S., Lim, F., Rembach, A., Rainey-Smith, S., Ames, D., Cobiac, L., Macaulay, SL., Masters, C., Rowe, C., Bush, A., Martins, R., (2015), Follow-up plasma apolipoprotein E levels in the Australian Imaging, Biomarkers and Lifestyle Flagship Study of Ageing (AIBL) cohort. Alzheimers Research and Therapy, 7(1), Article no.16, United Kingdom, BioMed Central Ltd., DOI: 10.1186/s13195-015-0105-6 ...
https://www.ecu.edu.au/schools/medical-and-health-sciences/our-staff/profiles/research-associates/mr-steve-pedrini
Core2 1-6-N-glucosaminyltransferase-I deficiency protects injured arteries from neointima formation in ApoE-deficient mice. |...  Core2 1-6-N-glucosaminyltransferase-I deficiency protects injured arteries from neointima formation in ApoE-deficient mice. |...
Core2 1-6-N-glucosaminyltransferase-I deficiency protects injured arteries from neointima formation in ApoE-deficient mice. - Huan Wang, Weiyu Zhang, Rong Tang, Robert P Hebbel, M Anna Kowalska, Chunxiang Zhang, Jamey D Marth, Minoru Fukuda, Chuhong Zhu, Yuqing Huo
http://www.curehunter.com/public/pubmed19372458.do
An MRI technique for the quantification of atherosclerotic lesions in the ApoE knockout mouse - Department of Pharmacology  An MRI technique for the quantification of atherosclerotic lesions in the ApoE knockout mouse - Department of Pharmacology
We use cookies to ensure that we give you the best experience on our website. If you click Continue well assume that you are happy to receive all cookies and you wont see this message again. Click Find out more for information on how to change your cookie settings ...
https://pharm.ox.ac.uk/publications/105450
Dr Anbu Thalamuthu | CHEBA - Centre for Healthy Brain Ageing  Dr Anbu Thalamuthu | CHEBA - Centre for Healthy Brain Ageing
Lipnicki DM; Crawford JD; Dutta R; Thalamuthu A; Kochan NA; Andrews G; Fernanda Lima-Costa M; Castro-Costa E; Brayne C; Matthews FE, 2017, Age-related cognitive decline and associations with sex, education and apolipoprotein E genotype across ethnocultural groups and geographic regions: a collaborative cohort study, PLOS ONE, vol. 12, http://dx.doi.org/10.1371/journal.pmed.1002261. Opel N; Redlich R; Kaehler C; Grotegerd D; Dohm K; Heindel W; Kugel H; Thalamuthu A; Koutsouleris N; Arolt V, 2017, Prefrontal gray matter volume mediates genetic risks for obesity, Molecular Psychiatry, vol. 22, pp. 703 - 710, http://dx.doi.org/10.1038/mp.2017.51. Lipnicki DM; Crawford JD; Dutta R; Thalamuthu A; Kochan NA; Andrews G; Lima-Costa MF; Castro-Costa E; Brayne C; Matthews FE, 2017, Age-related cognitive decline and associations with sex, education and apolipoprotein E genotype across ethnocultural groups and geographic regions: a collaborative cohort study, PLoS Medicine, vol. 14, ...
https://cheba.unsw.edu.au/people/dr-anbu-thalamuthu
Cytochrome P450 1B1 Contributes to the Development of Atherosclerosis and Hypertension in Apolipoprotein E-Deficient...  Cytochrome P450 1B1 Contributes to the Development of Atherosclerosis and Hypertension in Apolipoprotein E-Deficient...
This study demonstrated that CYP1B1 is critical for the development of AAL, associated inflammation, vascular damage, and hypertension in ApoE−/− mice fed AD, most likely by promoting increased oxidative stress and hyperlipidemia, which seems to be independent of lipid absorption. Eight-week-old ApoE−/−/Cyp1b1+/+ mice fed AD but not ND for 12 weeks developed AAL in the descending thoracic and abdominal aorta and in sections of proximal aorta. Our finding, that treatment with TMS, an inhibitor of CYP1B1 activity,19 for 12 weeks in ApoE−/−/Cyp1b1+/+ mice fed AD minimized AAL, suggests that CYP1B1 activity is required for the development of lesions. Although CYP1B1 is constitutively active, AD increased CYP1B1 activity without altering its expression as measured in the heart, whereas TMS inhibited its activity but not its expression. Because CYP1B1 is constitutively active, the increase in its activity by AD that could be because of biochemical modification of this enzyme remains to be ...
http://hyper.ahajournals.org/content/67/1/206
Treatment Online  Treatment Online
A recent article in this month s Archives of General Psychiatry underscores all this hoopla about the Apo E4 alleles. Apolipoprotein E Genotype and Age-Related Mylein Breakdown in Healthy Individuals by George Bartzokis M.D. et al. These authors discuss that In addition to genotype-phenotype associations with vascular disease, the alleles and isoforms of Apo E4 have been related to dementias, most commonly Alzheimer s disease. Apolipoprotein E (APOE) genotype is the most influential Alzheimer disease (AD) risk factor after advanced age. The APOE4 alleles decrease and the APOE2 alleles increase age at onset of AD. Human and nonhuman primate data suggest that in midlife, the structural integrity of myelin sheaths begins breaking down, with an accelerating age-related trajectory most evident in the brains later-myelinating association regions. This may result in a progressive "disconnection" of widely distributed neural networks that may underlie the age risk factor for AD. The authors of this ...
http://www.treatmentonline.com/blog/index.asp?blog_id=354
Knockdown of microRNA-17-5p ameliorates atherosclerotic lesions in ApoE−/− mice and restores the expression of very low density...  Knockdown of microRNA-17-5p ameliorates atherosclerotic lesions in ApoE−/− mice and restores the expression of very low density...
Objective To propose and verify a hypothesis that miR-17-5p knockdown may mitigate atherosclerotic lesions using atherosclerotic ApoE−/−mice as serum microRNA-17-5p (miR-17-5p) is elevated in...
https://link.springer.com/article/10.1007/s10529-017-2337-y
AG16714  AG16714
ARG158CYS; The 3 major isoforms of human apolipoprotein E (apoE2, -E3, and -E4), as identified by isoelectric focusing, are coded for by 3 alleles (epsilon 2, 3, and 4). The E2 (107741.0001), E3 (107741.0015), and E4 (107741.0016) isoforms differ in amino acid sequence at 2 sites, residue 112 (called site A) and residue 158 (called site B). At sites A/B, apoE2, -E3, and -E4 contain cysteine/cysteine, cysteine/arginine, and arginine/arginine, respectively [Weisgraber et al. J. Biol. Chem. 256: 9077-9083 (1981) and Rall et al. Proc. Nat. Acad. Sci. 79: 4696-4700 (1982 ...
https://coriell.org/0/Sections/Search/Sample_Detail.aspx?Ref=AG16714&PgId=166
SpectraCell Laboratories Offers Apolipoprotein E Genetic Testing  SpectraCell Laboratories Offers Apolipoprotein E Genetic Testing
Effective immediately, SpectraCell Laboratories now offers apolipoprotein E genotyping. This test determines a persons genetic risk for heart disease associated with the commonly
http://www.medindia.net/health-press-release/SpectraCell-Laboratories-Offers-Apolipoprotein-E-Genetic-Testing-67709-1.htm
Genetic variant determines prognosis after heart attack  Genetic variant determines prognosis after heart attack
Director of the J. David Gladstone Institutes, cardiologist Robert Mahley, a leading expert on apoE, calls the study an important research observation. "It indicates that there may be subgroups of patients who respond differently to statins, and this is especially interesting in relation to the continuing search for the mechanisms of apoE." As yet, F rgeman admits, the researchers "cannot explain our findings in terms of the underlying biology." One initial hypothesis was that there was a connection to patients levels of cholesterol and other lipids in the blood, but data analysis revealed this was not the case. The team now suspects the apoE protein to be involved in some malignant pathogenic processes that lead to coronary death. Results of earlier studies have suggested that e4 carriers are particularly prone to develop disseminated coronary lesions. "We think it most likely that our observations reflect an ability of statin treatment to inhibit the progression of such lesions in e4 ...
http://www.genomenewsnetwork.org/articles/06_00/genetic_heart_attack.shtml
Sherral Devine | School of Medicine  Sherral Devine | School of Medicine
Published on 10/1/2017. Neu SC, Pa J, Kukull W, Beekly D, Kuzma A, Gangadharan P, Wang LS, Romero K, Arneric SP, Redolfi A, Orlandi D, Frisoni GB, Au R, Devine S, Auerbach S, Espinosa A, Boada M, Ruiz A, Johnson SC, Koscik R, Wang JJ, Hsu WC, Chen YL, Toga AW. Apolipoprotein E Genotype and Sex Risk Factors for Alzheimer Disease: A Meta-analysis. JAMA Neurol. 2017 Oct 01; 74(10):1178-1189. PMID: 28846757.. Read at: PubMed ...
https://www.bumc.bu.edu/busm/profile/sherral-devine/
mylab | 細胞因子 / APOE4 Human; Apolipoprotein E4 Human Recombinant 100µg  mylab | 細胞因子 / APOE4 Human; Apolipoprotein E4 Human Recombinant 100µg
Amino Acid SequenceMHHHHHHKVE QAVETEPEPE LRQQTEWQSG QRWELALGRF WDYLRWVQTL SEQVQEELLS SQVTQELRAL MDETMKELKA YKSELEEQLT PVAEETRARL SKELQAAQAR LGADMEDVRG RLVQYRGEVQ AMLGQSTEEL RVRLASHLRK LRKRLLRDAD DLQKRLAVYQ AGAREGAERG LSAIRERLGP LVEQGRVRAA TVGSLAGQPL QERAQAWGER LRARMEEMGS RTRDRLDEVK EQVAEVRAKL EEQAQQIRLQ AEAFQARLKS WFEPLVEDMQ RQWAGLVEKV QAAVGTSAAP VPSDNH.DescriptionApolipoprotein E4 Human Recombinant produced in E.coli is a single, non-glycosylated polypeptide chain containing a total of 306 amino acids including a His Tag at N-terminus and having a molecular mass of 35.2kDa. The Accession # is P02649 VAR_000652.FormulationLyophilized from a sterile (0.2µm) filtered aqueous solution containing 10mM sodium phosphate, pH 7.5.Physical AppearanceSterile Filtered White lyophilized (freeze-dried) powder.PurityGreater than 90% as determined by SDS-PAGE.SolubilityIt is recommended to reconstitute the lyophilized APOE4 in sterile 18M-cm H2O not less than 100µg/ml, which can then be further diluted to other
https://www.mylab.com.tw/products/cyt-968-apoe4-human-apolipoprotein-e4-human-recombinant-100-g
Preventive Strategies - India ElderConnect  Preventive Strategies - India ElderConnect
Researchers have identified a protein called apolipoprotein E (ApoE) which affects your chances of developing Alzheimers disease. There are three forms of ApoE: ApoE2, ApoE3 and ApoE4.. Having one or two copies of ApoE4 increases someones chance of developing the disease, but does not make it certain. Some researchers think that ApoE4 does not affect whether a person will get the disease but, rather, when they get it, causing people with ApoE4 to develop the disease before people with ApoE2.. ...
http://indiaelderconnect.com/preventive-strategies-for-dementia/
Three-dimensional DPC imaging of an ex-vivo ApoE−/− | Open-i  Three-dimensional DPC imaging of an ex-vivo ApoE−/− | Open-i
Three-dimensional DPC imaging of an ex-vivo ApoE−/− mouse heart.(A-C) The three principal axes of the heart give a clear overview of the global structure
https://openi.nlm.nih.gov/detailedresult.php?img=PMC4499839_srep11980-f1&req=4
Apolipoprotein E phenotypes in patients with gout: relation with hypertriglyceridaemia. | Annals of the Rheumatic Diseases  Apolipoprotein E phenotypes in patients with gout: relation with hypertriglyceridaemia. | Annals of the Rheumatic Diseases
OBJECTIVE--To elucidate the relationship, if any, between lipid abnormalities and apolipoprotein E (apo E) polymorphism, by investigating apo E phenotype and allele frequency. METHODS--Fasting blood samples were taken for determination of apo E phenotype and serum lipids in 221 male patients with gout and 141 control male subjects. Apo E phenotype was determined by one dimensional flat gel isoelectric focusing. RESULTS--Frequencies of apo E phenotypes in gout were apo E3/3 67.9%, E4/3 18.1%, E4/4 2.3%, E4/2 1.8%, E3/2 9.5%, and E2/2 0.5%; those in control male subjects were 74.5%, 15.6%, 0%, 1.4%, 7.1%, and 1.4%, respectively. Frequencies of the e2, e3, and e4 alleles in gout were 0.061, 0.817 and 0.122, compared with the corresponding control frequencies of 0.057, 0.858 and 0.085. These differences in apo E phenotype and allele frequencies between gout and control subjects were not significant. The frequency of apo e4 allele in hyperlipidaemic gout subjects was significantly greater than that ...
http://ard.bmj.com/content/54/5/351
Innate immune recognition of invasive bacteria accelerates atherosclerosis in apolipoprotein E-deficient mice<...  Innate immune recognition of invasive bacteria accelerates atherosclerosis in apolipoprotein E-deficient mice<...
TY - JOUR. T1 - Innate immune recognition of invasive bacteria accelerates atherosclerosis in apolipoprotein E-deficient mice. AU - Gibson, Frank C.. AU - Hong, Charlie. AU - Chou, Hsin H.. AU - Yumoto, Hiromichi. AU - Chen, Jiqiu. AU - Lien, Egil. AU - Wong, Jodie. AU - Genco, Caroline Attardo. PY - 2004/6/8. Y1 - 2004/6/8. N2 - Background - Infectious diseases have emerged as potential risk factors for cardiovascular disease (CVD). Epidemiological studies support a connection between periodontal disease, a chronic inflammatory disease of the supporting tissues of the teeth, and CVD. Methods and Results - To directly test the connection between periodontal disease and atherosclerosis, apoE-/- mice were orally challenged with the periodontal disease pathogen Porphyromonas gingivalis or an invasion-impaired P gingivalis fimbriae-deficient mutant (FimA-). Both wild-type P gingivalis and the FimA- mutant were detected in blood and aortic arch tissue of apoE-/- mice by PCR after challenge. ApoE-/- ...
https://tmu.pure.elsevier.com/en/publications/innate-immune-recognition-of-invasive-bacteria-accelerates-athero
Inflammatory And Epithelial Changes In Lungs From Apolipoprotein E Deficient Mice After Chronic Cigarette Mainstream Smoke...  Inflammatory And Epithelial Changes In Lungs From Apolipoprotein E Deficient Mice After Chronic Cigarette Mainstream Smoke...
Inflammation plays a key role in the atherosclerotic process. As part of a study on the influence of cigarette mainstream smoke (ms) in combination with high-fat diet on the development of atherosclerosis, we investigated the inflammatory response and histopathological alterations in lungs from Apolipoprotein E-deficient (ApoE -/-) mice, a classic model for atherosclerosis. Male ApoE -/- mice were whole-body exposed for 12 months (6 h/d, 5 d/wk) to diluted MS at total particulate matter (TPM) concentrations of 100 and 200 μg/l or to filtered fresh air. Each exposure group was fed either a chow diet or a milk-fat-enriched diet. Bronchoalveolar lavage (BAL) was performed and inflammatory cells were quantified in BAL fluid (BALF); lungs were evaluated histopathologically. Mice exposed to 100 μg TPM/l MS showed no statistically significant inflammatory and epithelial changes in the lung. Mice exposed to 200 μg TPM/l MS showed statistically significant inflammatory changes, i.e., a constant ...
https://www.pmiscience.com/library/publication/inflammatory-and-epithelial-changes-in-lungs-from-apolipoprotein-e-deficient-mice-after-chronic-cigarette-mainstream-smoke-exposure
Apolipoprotein E polymorphism in American Indians and its relation to plasma lipoproteins and diabetes: The Strong Heart Study  Apolipoprotein E polymorphism in American Indians and its relation to plasma lipoproteins and diabetes: The Strong Heart Study
Effect of tocopherol on atherosclerosis, vascular function, and inflammation in apolipoprotein E knockout mice with subtotal...  Effect of tocopherol on atherosclerosis, vascular function, and inflammation in apolipoprotein E knockout mice with subtotal...
Following 12 weeks, in vitro aortic endothelial-independent relaxation was enhanced with both α-tocopherol and mixed-tocopherol (P , 0.05), while mixed-tocopherol enhanced aortic contraction at noradrenaline concentrations of 3 × 10−7 M to 3 × 10−5 M (P , 0.05), when compared to normal chow. Supplementation with α- and mixed-tocopherol reduced systemic concentrations of IL-6 (P , 0.001 and P , 0.001, respectively) and IL-10 (P , 0.05 and P , 0.001, respectively), while α-tocopherol also reduced MCP-1 (P , 0.05) and tumor necrosis factor (TNF)-α (P , 0.05). Aortic sinus plaque area was significantly reduced with α-tocopherol supplementation when compared to normal chow (P , 0.01 ...
https://espace.library.uq.edu.au/view/UQ:348789
Apolipoprotein E4 allele as a predictor of cholinergic deficits and treatment outcome in Alzheimer disease | PNAS  Apolipoprotein E4 allele as a predictor of cholinergic deficits and treatment outcome in Alzheimer disease | PNAS
Apolipoprotein E (apoE) is critical in the modulation of cholesterol and phospholipid transport between cells of different types. Human apoE is a polymorphic protein with three common alleles, APO epsilon 2, APO epsilon 3, and APO epsilon 4. ApoE4 is associated with sporadic and late-onset familial Alzheimer disease (AD). Gene dose was shown to have an effect on risk of developing AD, age of onset, accumulation of senile plaques in the brain, and reduction of choline acetyltransferase (ChAT) activity in the hippocampus of AD subjects. To characterize the possible impact of the apoE4 allele on cholinergic markers in AD, we examined the effect of apoE4 allele copy number on pre- and postsynaptic markers of cholinergic activity. ApoE4 allele copy number showed an inverse relationship with residual brain ChAT activity and nicotinic receptor binding sites in both the hippocampal formation and the temporal cortex of AD subjects. AD cases lacking the apoE4 allele showed ChAT activities close or within ...
https://www.pnas.org/content/92/26/12260?ijkey=8db609a2ef1c585197232112a720d4975e521d2d&keytype2=tf_ipsecsha
Avian and murine lr8b and human apolipoprotein E receptor 2: Differentially spliced products from corresponding genes<...  Avian and murine lr8b and human apolipoprotein E receptor 2: Differentially spliced products from corresponding genes<...
TY - JOUR. T1 - Avian and murine lr8b and human apolipoprotein E receptor 2. T2 - Differentially spliced products from corresponding genes. AU - Brandes, Christian. AU - Novak, Sabine. AU - Stockinger, Walter. AU - Herz, Joachim. AU - Schneider, Wolfgang J.. AU - Nimpf, Johannes. PY - 1997/6/1. Y1 - 1997/6/1. N2 - Apolipoprotein E-mediated lipid metabolism in the central nervous system plays an important role in cholesterol and phospholipid homeostasis of this organ, which is separated from the circulation by the blood-brain barrier. Moreover, in late-onset familial Alzheimer disease the frequency of the apolipoprotein E4 allele is significantly increased and the apoprotein is localized to extracellular plaques, one of the histological hallmarks of this disease. Recently, two distinct novel members of the low-density lipoprotein (LDL) receptor family, with the potential to bind apolipoprotein E and preferentially expressed in brain, have been characterized from human (D. Kim et al., 1996, J. ...
https://utsouthwestern.pure.elsevier.com/en/publications/avian-and-murine-lr8b-and-human-apolipoprotein-e-receptor-2-diffe
北京大学医学部机构知识库(IR@PKUHSC): Hyperhomocysteinemia Exaggerates Adventitial Inflammation and Angiotensin II-Induced Abdominal Aortic...  北京大学医学部机构知识库([email protected]): Hyperhomocysteinemia Exaggerates Adventitial Inflammation and Angiotensin II-Induced Abdominal Aortic...
Rationale: A number of epidemiological studies have suggested an association of hyperhomocysteinemia (HHcy) and abdominal aortic aneurysm (AAA), but discrepancies exist. In addition, we lack direct evidence supporting a causal role.. Objective: We determined the association and contribution of HHcy to AAA formation.. Methods and Results: We first performed a meta-analysis of studies involving 1489 subjects and found a strong association of HHcy and AAA (odds ratio, 7.39). Next, we used angiotensin II-infused male apolipoprotein E-deficient mice and tested whether HHcy contributes to AAA pathogenesis. Homocysteine (Hcy) supplement (1.8 g/L) in drinking water resulted in mild HHcy. Intriguingly, HHcy greatly increased the incidence of angiotensin II-induced AAA and aortic dissection in apolipoprotein E-deficient mice (vehicle versus Hcy: 50% versus 100%; ...
http://ir.bjmu.edu.cn/handle/400002259/67393
Exposure to diesel exhaust up-regulates iNOS expression in ApoE knockout mice (Journal Article) | SciTech Connect  Exposure to diesel exhaust up-regulates iNOS expression in ApoE knockout mice (Journal Article) | SciTech Connect
Traffic related particulate matter air pollution is a risk factor for cardiovascular events; however, the biological mechanisms are unclear. We hypothesize that diesel exhaust (DE) inhalation induces up-regulation of inducible nitric oxide synthase (iNOS), which is known to contribute to vascular dysfunction, progression of atherosclerosis and ultimately cardiovascular morbidity and mortality. Methods: ApoE knockout mice (30-week) were exposed to DE (at 200 {mu}g/m{sup 3} of particulate matter) or filtered-air (control) for 7 weeks (6 h/day, 5 days/week). iNOS expression in the blood vessels and heart was evaluated by immunohistochemistry and western blotting analysis. To examine iNOS activity, thoracic aortae were mounted in a wire myograph, and vasoconstriction stimulated by phenylephrine (PE) was measured with and without the presence of the specific inhibitor for iNOS (1400 W). NF-{kappa}B (p65) activity was examined by ELISA. The mRNA expression of iNOS and NF-{kappa}B (p65) was determined ...
https://www.osti.gov/scitech/biblio/21587826
New aspects in the pathogenesis of diabetic atherothrombosis | JACC: Journal of the American College of Cardiology  New aspects in the pathogenesis of diabetic atherothrombosis | JACC: Journal of the American College of Cardiology
The HDLs are responsible for the removal of free cholesterol from the blood. Low plasma levels of HDL are associated with increased cardiovascular risk. Low levels of HDL are frequently seen in patients with insulin resistance, from the metabolic syndrome to overt diabetes mellitus. Badimon et al. (59,60) elegantly demonstrated the antiatherogenic properties of HDL, reducing the number of fatty streaks and inducing disease regression in the rabbit experimental model. More recently, Rong et al. (61) evaluated the effects of HDL in advanced experimental atherosclerosis. Diseased thoracic aortic segments from hypercholesterolemic apolipoprotein E-deficient mice were transplanted in the abdominal aorta of apolipoprotein E-deficient mice not expressing (plasma HDL cholesterol approximately 26 mg/dl) or expressing (HDL approximately 64 mg/dl) a human apolipoprotein AI transgene. Mice with high plasma HDL showed significant changes in plaque composition, with macrophage area reductions ,80% and ...
http://www.onlinejacc.org/content/44/12/2293
Serine Protease Inhibitor Serp-1 Strongly Impairs Atherosclerotic Lesion Formation and Induces a Stable Plaque Phenotype in...  Serine Protease Inhibitor Serp-1 Strongly Impairs Atherosclerotic Lesion Formation and Induces a Stable Plaque Phenotype in...
In this study, the effect of the myxoma virus-derived serine protease inhibitor Serp-1 was investigated on de novo atherosclerosis and on advanced atherosclerotic lesions in apoE−/− mice equipped with a perivascular collar to induce carotid artery lesions.28 Serp-1 treatment led to a striking reduction in de novo lesion formation, whereas Serp-1 did not affect plasma total cholesterol and triglyceride levels as well as the total body weight of the animals or promote outward remodeling of the carotid artery. Plasma levels of Serp-1 after subcutaneous infusion remained constant during treatment at approximately 13.5 pmol/L. These low picomolar Serp-1 levels have been reported to suffice for effective serine protease inhibition and for blocking the hosts immune response to myxoma infection.20,21 Further gel filtration analysis revealed that Serp-1 was not degraded during the timeframe of the experiment. Blood cell levels did not differ between control and Serp-1 treatment groups, suggesting ...
http://circres.ahajournals.org/content/93/5/464
Full text] Role of apolipoprotein E in neurodegenerative diseases | NDT  Full text] Role of apolipoprotein E in neurodegenerative diseases | NDT
Role of apolipoprotein E in neurodegenerative diseases Vo Van Giau,1 Eva Bagyinszky,1 Seong Soo A An,1 SangYun Kim2 1Department of Bionano Technology, Gachon Medical Research Institute, Gachon University, Seongnam, South Korea; 2Department of Neurology, Seoul National University College of Medicine in Seoul National Bundang Hospital, Seoul, South Korea Abstract: Apolipoprotein E (APOE) is a lipid-transport protein abundantly expressed in most neurons in the central nervous system. APOE-dependent alterations of the endocytic pathway can affect different functions. APOE binds to cell-surface receptors to deliver lipids and to the hydrophobic amyloid-β peptide, regulating amyloid-β aggregations and clearances in the brain. Several APOE isoforms with major structural differences were discovered and shown to influence the brain lipid transport, glucose metabolism, neuronal signaling, neuroinflammation, and mitochondrial function. This review will summarize the updated research progress on APOE functions
https://www.dovepress.com/role-of-apolipoprotein-e-in-neurodegenerative-diseases-peer-reviewed-fulltext-article-NDT
Quantification of total apolipoprotein E and its isoforms in cerebrospinal fluid from patients with neurodegenerative diseases ...  Quantification of total apolipoprotein E and its isoforms in cerebrospinal fluid from patients with neurodegenerative diseases ...
The human APOE gene, which codes for apolipoprotein E (apoE), has three major polymorphic alleles: ε2, ε3, and ε4 that give rise to amino acid substitutions. APOE-ε4 is a strong risk factor of sporadic Alzheimers disease (AD) but the reason why is still unknown despite intense research for more than 20 years. The aim of the study was to investigate if the concentrations of total apoE and the specific apoE isoforms in cerebrospinal fluid (CSF) differ between various neurodegenerative diseases and control individuals, as well as among the APOE genotypes. Quantification of total apoE and specific apoE isoforms (E2, E3, and E4) in CSF was performed using high-resolution parallel reaction monitoring mass spectrometry. In total, 1820 individuals were involved in the study including clinically diagnosed AD patients (n = 228), cognitively unimpaired (CU) patients (n = 896), and patients with other neurodegenerative disorders (n = 696). Follow-up data was available for 100 individuals, assessed at two time
https://alzres.biomedcentral.com/articles/10.1186/s13195-020-00585-7
Do Apolipoprotein E Polymorphisms Influence Risk of Cognitive Decline by Modulating Omega-3 Fatty Acid Metabolism? - Full Text...  Do Apolipoprotein E Polymorphisms Influence Risk of Cognitive Decline by Modulating Omega-3 Fatty Acid Metabolism? - Full Text...
BACKGROUND: Compared to the epsilon 2 or epsilon 3 alleles, the epsilon 4 allele of apolipoprotein E (ApoE4) is associated with twice the prevalence of late-onset Alzheimers disease (AD). Epidemiological studies show that risk of AD varies inversely with consumption of omega-3 fatty acids from fish and seafood. Despite apparently lower fish intake in AD, pooled analysis of the literature shows that plasma and brain docosahexaenoic acid (DHA) is actually the same in AD as in healthy age-matched controls. Fish oil trials in AD are also not convincing. We recently shown that ApoE4 carriers have 41% higher fasting plasma EPA and DHA compared to non-carriers, but the plasma EPA and DHA response to fish oil in ApoE4 carriers was half that seen in non-carriers.. HYPOTHESES: (i) Carriers of ApoE4 have altered metabolism of carbon-13 (13C)-DHA as well as EPA and DHA provided in a dietary supplement. (ii) A dietary supplement of EPA+DHA will improve cognitive performance but only in non-carriers of ...
https://clinicaltrials.gov/ct2/show/NCT01577004
Total silicon concentration of the aorta of female apoE | Open-i  Total silicon concentration of the aorta of female apoE | Open-i
Total silicon concentration of the aorta of female apoE knockout mice in Study 1 fed a diet high in butter fat and depleted in silicon, compared with mice fed t
https://openi.nlm.nih.gov/detailedresult.php?img=PMC4478943_jn206193fig3&req=4
Large-scale evidence that the cardiotoxicity of smoking is not significantly modified by the apolipoprotein E epsilon2/epsilon3...  Large-scale evidence that the cardiotoxicity of smoking is not significantly modified by the apolipoprotein E epsilon2/epsilon3...
Results from two small studies, involving a total of only 174 cases, have suggested that the increased risk of coronary heart disease conferred by cigarette smoking is substantially affected by genotype at the apolipoprotein E (APOE) epsilon2/epsilon3/epsilon4 polymorphism. We have established APOE genotypes in 4484 patients with acute myocardial infarction diagnosed before the age of 55 years for male and 65 years for female patients, and in 5757 controls with no history of cardiovascular disease. On average, the hazard ratio for myocardial infarction was 1.17 (95% CI 1.09-1.25; p|0.00001) per stepwise change from epsilon3/2 to epsilon3/3 to epsilon3/4 genotype. Among individuals in this study with known cigarette smoking status, the hazard ratio for myocardial infarction in smokers versus non-smokers was 4.6 (4.2-5.1). There was, however, no significant difference between the smoker/non-smoker hazard ratios for those with different APOE genotypes (chi2(2)=0.69; p=0.7). When differences in risk between
https://www.ctsu.ox.ac.uk/publications/38534
Lack of interleukin-1ß decreases the severity of atherosclerosis in apoE-deficient mice<...  Lack of interleukin-1ß decreases the severity of atherosclerosis in apoE-deficient mice<...
TY - JOUR. T1 - Lack of interleukin-1ß decreases the severity of atherosclerosis in apoE-deficient mice. AU - Kirii, Hirokazu. AU - Niwa, Tamikazu. AU - Yamada, Yasuhiro. AU - Wada, Hisayasu. AU - Saito, Kuniaki. AU - Iwakura, Yoichiro. AU - Asano, Masahide. AU - Moriwaki, Hisataka. AU - Seishima, Mitsuru. PY - 2003/4/1. Y1 - 2003/4/1. N2 - Objective - Atherosclerosis is considered to be a chronic inflammatory disease and many cytokines participate in the development of atherosclerosis, We focused on the role of interleukin-1β (IL-1β, one of the proinflammatory cytokines secreted by monocytes/macrophages, in the progression of atherosclerosis. Methods and Results - We generated mice lacking both apoE and IL-1β. The sizes of atherosclerotic lesions at the aortic sinus in apoE-/-/IL-1β-/- mice at 12 and 24 weeks of age showed a significant decrease of approximately 30% compared with apoE-/-/IL-1β+/+ mice, and the percentage of the atherosclerotic area to total area of apoE-/-/IL-1β-/- at 24 ...
https://pure.fujita-hu.ac.jp/en/publications/lack-of-interleukin-1%C3%9F-decreases-the-severity-of-atherosclerosis-
The Rockefeller University » Hospital Centennial  The Rockefeller University » Hospital Centennial
Today more than 95 percent of experimental pathology research in atherosclerosis is carried out using the apo E knockout mouse. Not only has it provided a system for studying how lesions form in arteries, it also has given scientists a way to test the effects of other genes on how atherosclerosis develops, by breeding so-called candidate genes onto the apo E knockout mouse background. In addition, when Breslow crossed the apo E knockout trait onto different inbred mouse strains, he found a wide range in the size of the lesions that formed. This indicated modifier genes, and through genetic crosses he has found additional genes involved in atherosclerosis susceptibility. The apo E knockout mouse is also widely used in the pharmaceutical industry to test compounds for treating atherosclerosis. Jan L. Breslow received the AB from Columbia College (1963), the MA from Columbia University (1964), and the MD from Harvard Medical School (1968). After an internship and residency in pediatrics at Boston ...
http://centennial.rucares.org/index.php?page=Heart-Attack_Mouse
Expression of Reg IV in inflammatory bowel disease and the predictive effect on lesion activity  Expression of Reg IV in inflammatory bowel disease and the predictive effect on lesion activity
Plus it  Plus it
Melanoma is the most aggressive skin cancer due to a propensity to metastasize and resistance to standard therapies. Nuclear hormone receptors are therapeutic targets in reproductive tissues, but their clinical utility in other solid tumors such as melanoma remains undefined. Pencheva and colleagues observed that liver-X nuclear hormone receptor β (LXRβ) was ubiquitously expressed across patient-derived melanoma cell lines and that LXR agonists inhibited invasion and endothelial cell recruitment of multiple melanoma cell lines in vitro in an LXRβ-dependent manner. Furthermore, oral administration of LXR agonists suppressed melanoma xenograft tumor growth, accompanied by a reduction in the number and size of tumoral endothelial vessels as well as lung and brain metastases. LXRβ is a known transcriptional activator of the metastasis suppressor apolipoprotein-E (ApoE), and extracellular ApoE was shown to be the primary mediator of tumor suppression by activated LXR, as antibody-mediated ...
http://cancerdiscovery.aacrjournals.org/content/early/2014/03/12/2159-8290.CD-RW2014-056
Frequency distribution of apolipoprotein e genotypes in elderly Han Chinese population and relationship with senile dementia -...  Frequency distribution of apolipoprotein e genotypes in elderly Han Chinese population and relationship with senile dementia -...
RESULTS: We found that the most prevalent genotype was Apo Eε3/3, followed in order by Apo Eε3/4 and Apo Eε2/2. The estimated ApoE allelic frequencies in individuals with SD were 0.095, 0.560, and 0.345 for ε2, ε3, and ε4, respectively. In controls, the corresponding Apo E allelic frequencies were 0.146, 0.699, and 0.155. The percentage of ε4 allele carriers in SD group was significantly higher than that in control group ( ...
https://www.minervamedica.it/it/riviste/neurosurgical-sciences/articolo.php?cod=R38Y9999N00A140043
BLMH and APOE genes in Alzheimer Disease: A possible relation  BLMH and APOE genes in Alzheimer Disease: A possible relation
ABSTRACT. Alzheimer disease (AD) is a progressive and irreversible neurodegenerative disorder that is characterized by cognitive decline, memory loss and confusion. The E4 allele of the apolipoprotein E gene (APOE) is associated with AD and it is the main genetic risk factor for disease. Although the exact physiological function is unknown, bleomycin hydrolase (BLMH) may also be associated with AD development, although previous immunohistochemical findings have been inconsistent. Therefore, the purpose of this study was to evaluate the genotypic and allele frequencies of the APOE gene and BLMH 1450 G > A polymorphism and assess BLMH expression using PCR-RFLP and RT-qPCR analyses of blood samples from patients with Alzheimer disease (AD), healthy elderly adults (EC) and healthy young subjects (YC). BLMH expression was significantly different among groups (p = 0.015) and there was substantial reduction with age and with AD. The APOE and BLMH genotype frequency did not diverge from the ...
https://file.scirp.org/Html/6-2440038_37292.htm
EFFECTS OF FCγRIIIA ON AORTIC ATHEROSCLEROTIC PLAQUE DESTABILISATION IN APOE−/− MICE | Heart  EFFECTS OF FCγRIIIA ON AORTIC ATHEROSCLEROTIC PLAQUE DESTABILISATION IN APOE−/− MICE | Heart
Methods Twenty wt C57BL/6J mice were chosen as the control group, and 60 ApoE−/− mice were randomly divided into three groups, ApoE−/− group, ApoE−/−+ IVIG group, ApoE−/−+ Simvastatin (Sm) group, with 20 mice in each group. Mice in ApoE−/−+IVIG group received an intraperitoneal injection of IVIG (1 mg/g) daily over a 5-day period prior to the exposure to high-fat diet. Mice in the ApoE−/−+Sm group received Sm (0.026 g/kg) per gavage for 10 weeks. Mice in C57 group and ApoE−/− group received PBS. Pathomorphological changes of aorta were observed by Masson staining evaluating plaques collagen content, immunohistochemical staining α-actin and CD68 evaluating contents of plaques vascular smooth muscle cells and macrophages, and oil red O staining evaluating plaques adipose tissue contents. FcγRIIIA expression changes in mice with atherosclerotic plaque were determined by assaying the protein level of membrane CD16 on monocytes using immunofluorescent staining and FACS ...
http://heart.bmj.com/content/98/Suppl_2/E70.3
NICM | Sai Seto  NICM | Sai Seto
Emeto T, Seto SW, Golledge J. Targets for medical therapy to limit abdominal aortic aneurysm progress. Curr Drug Targets (2014) 15(9): 860-873. Wang Y, Emeto T, Lee J, Marshman L, Moran C, Seto SW, Golledge J. Mouse modes of intracranial aneurysm. Brain Pathology (2014) Accepted Manuscript.. Seto SW, Krishna SM, Moran CS, Liu D, Golledge J. Aliskiren limits abdominal aortic aneurysm, ventricular hypertrophy and atherosclerosis in an apolipoprotein E deficient mouse model. Clin Sci (Lond) (2014) 127(2): 123-34.. Wang Y, Seto SW, Golledge J. Angiotensin II, sympathetic nerve activity and chronic heart failure. Heart Failure Reviews (2014) 19(2): 187-198.. 2013. Clancy P, Seto SW, Koblar SA, Golledge J. Role of angiotensin converting enzyme 1/angiotensin II/ angiotensin receptor 1 axis in interstitial collagenase expression in human carotid atheroma. Atherosclerosis (2013) 229(2): 331-337.. Seto SW, Au AL, Poon CC, Zhang Q, Li RW, Yeung JH, Kong SK, Ngai SM, Wan S, Ho HP, Lee SM, Hoi MP, Chan SW, ...
http://nicm.edu.au/about_us/people/researchers/sai_seto
EAS Newsletter  EAS Newsletter
Atherogenesis is initiated by subendothelial accumulation (i.e. retention) of apolipoprotein B (apoB)-containing lipoproteins. Lipoprotein retention only occurs in specific vascular areas and is mediated by artery wall proteoglycans in the innermost layer of the artery (the arterial intima). In particular, proteoglycans with elongated glycosaminoglycan chains seem to play a crucial role in this process. The retained lipoproteins subsequently provoke an inflammatory response that ultimately leads to atherosclerosis. Atherogenic lipoproteins specifically locate in areas of intimal hyperplasia, characterised by accumulation of vascular smooth muscle cells and extracellular matrix. This thickened intima appears to act as a depot for extracellular lipids in the earliest initial stages of atherosclerosis. Furthermore, accumulation of apoB-containing triglyceride-rich lipoproteins in the postprandial state promotes the retention of remnant particles in the artery wall, in turn leading to accelerated ...
http://eas2015.kenes.com/latest-news/eas-newsletter
EAS Newsletter  EAS Newsletter
Atherogenesis is initiated by subendothelial accumulation (i.e. retention) of apolipoprotein B (apoB)-containing lipoproteins. Lipoprotein retention only occurs in specific vascular areas and is mediated by artery wall proteoglycans in the innermost layer of the artery (the arterial intima). In particular, proteoglycans with elongated glycosaminoglycan chains seem to play a crucial role in this process. The retained lipoproteins subsequently provoke an inflammatory response that ultimately leads to atherosclerosis. Atherogenic lipoproteins specifically locate in areas of intimal hyperplasia, characterised by accumulation of vascular smooth muscle cells and extracellular matrix. This thickened intima appears to act as a depot for extracellular lipids in the earliest initial stages of atherosclerosis. Furthermore, accumulation of apoB-containing triglyceride-rich lipoproteins in the postprandial state promotes the retention of remnant particles in the artery wall, in turn leading to accelerated ...
http://eas2015.kenes.com/Pages/EAS-Newsletter.aspx
Regional serum cholesterol differences in Belgium : do genetically determined cardiovascular risk factors contribute ? | Base...  Regional serum cholesterol differences in Belgium : do genetically determined cardiovascular risk factors contribute ? | Base...
Background Differences in serum lipid distribution and mortality from ischaemic heart disease have repeatedly been reported between Belgian northerners and southerners. We investigated whether serum lipoprotein a Lp a and apolipoprotein apo E polymorphism were involved. Methods Fasting serum lipids, apo A-I and B, and Lp a levels were examined...
http://www.bdsp.ehesp.fr/Base/173182/
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Browsing publications of the work group experimental Virology([TC]EVIR) by Submit Date  Browsing publications of the work group experimental Virology([TC]EVIR) by Submit Date
Hepatitis C virus (HCV) is extraordinarily diverse and uses entry factors in a strain-specific manner. Virus particles associate with lipoproteins, and apolipoprotein E (ApoE) is critical for HCV assembly and infectivity. However, whether ApoE dependency is common to all HCV genotypes remains unknown. Therefore, we compared the roles of ApoE utilizing 10 virus strains from genotypes 1 through 7. ApoA and ApoC also support HCV assembly, so they may contribute to virus production in a strain-dependent fashion. Transcriptome sequencing (RNA-seq) revealed abundant coexpression of ApoE, ApoB, ApoA1, ApoA2, ApoC1, ApoC2, and ApoC3 in primary hepatocytes and in Huh-7.5 cells. Virus production was examined in Huh-7.5 cells with and without ApoE expression and in 293T cells where individual apolipoproteins (ApoE1, -E2, -E3, -A1, -A2, -C1, and -C3) were provided in trans All strains were strictly ApoE dependent. However, ApoE involvement in virus production was strain and cell type specific, because some ...
https://repository.helmholtz-hzi.de/handle/10033/620590/browse?type=dateaccessioned
Effects of chronic treatment with L-arginine on atherosclerosis in apoE knockout and apoE/inducible NO synthase double-knockout...  Effects of chronic treatment with L-arginine on atherosclerosis in apoE knockout and apoE/inducible NO synthase double-knockout...
Sigma-Aldrich offers abstracts and full-text articles by [Jiqiu Chen, Peter Kuhlencordt, Fumi Urano, Hiroshi Ichinose, Joshua Astern, Paul L Huang].
https://www.sigmaaldrich.com/catalog/papers/12524231
ALZFORUM | NETWORKING FOR A CURE  ALZFORUM | NETWORKING FOR A CURE
Compelling and widely accepted genetic evidence shows that the presence of one or more APOE4 genes is associated with more severe disease in Alzheimers, stroke, traumatic brain injury, multiple sclerosis, and many others. The question is, How does APOE4/ApoE4 protein contribute to disease or conversely, how does the absence of APOE3/ApoE3 protein contribute to disease? The likely explanations are quantity and quality of ApoE differs between APOE4 carriers and non-APOE4 carriers (i.e., APOE3 carriers). Riddell and colleagues confirm, as we had previously reported (Vitek et al., 2007), that the amount of ApoE protein in APOE4/4 targeted replacement (TR) mice appears to be significantly less than in their APOE3/3 counterparts. Thus, like many diseases where some critical factor is reduced in the disease, a critical therapeutic path becomes supplementation of that missing critical factor with either the authentic protein or a mimetic of that protein.. But in the case of ApoE, amount is not the ...
http://www.alzforum.org/papers/impact-apolipoprotein-e-apoe-polymorphism-brain-apoe-levels
Apolipoprotein E 抗体(FITC)|Abcam中国|Anti-Apolipoprotein E 抗体(FITC)  Apolipoprotein E 抗体(FITC)|Abcam中国|Anti-Apolipoprotein E 抗体(FITC)
FITC偶联Apolipoprotein E 抗体(ab27613)可与人样本反应并经ICC/IF实验严格验证，实验条件参看说明书。Abcam对所有产品均提供质保服务和专属技术支持，中国75%以上现货。
http://www.abcam.cn/apolipoprotein-e-antibody-fitc-ab27613.html
Cyclooxygenase-2 inhibitors and atherosclerosis | JACC: Journal of the American College of Cardiology  Cyclooxygenase-2 inhibitors and atherosclerosis | JACC: Journal of the American College of Cardiology
It is surprising, therefore, that Rott et al. (1)found that inhibition of COX-2 aggravated atherosclerosis in the apoE knockout mouse. The study was more complex, as the authors set out to examine the effect of COX-2 inhibition on infectivity of cytomegalovirus and coincidentally showed increased disease burden in animals treated with the COX-2 inhibitor, including those not infected with the virus. Although it would be reasonable to conclude that this reflected selective suppression of PGI2and an unopposed effect of TXA2, the authors suggest as an alternative hypothesis the suppression of anti-inflammatory PGs, such as PGJ2, and its metabolite 15-deoxy-delta12,14-PGJ2(15d-PGJ2) (35).. Although COX-2 is usually thought of as contributing to inflammation, some authors have suggested that COX-2 may also play an anti-inflammatory role. The hypothesis arises from observations with COX-2 inhibitors and in animals in which the COX-2 gene has been disrupted. Although inducing an anti-inflammatory ...
http://www.onlinejacc.org/content/41/10/1820
Aorta of ApoE-Deficient Mice Responds to Atherogenic Stimuli by a Prelesional Increase and Subsequent Decrease in the...  Aorta of ApoE-Deficient Mice Responds to Atherogenic Stimuli by a Prelesional Increase and Subsequent Decrease in the...
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Gentaur Molecular :AbD \ NATIVE HUMAN APOLIPOPROTEIN A1, Product Type Purified Protein, Specificity APOLIPOPROTEIN A1, Target...  Gentaur Molecular :AbD \ NATIVE HUMAN APOLIPOPROTEIN A1, Product Type Purified Protein, Specificity APOLIPOPROTEIN A1, Target...
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What is the advantage of knockout over gene therapy in mice model in order to st - General Lab Techniques - BioForum  What is the advantage of knockout over gene therapy in mice model in order to st - General Lab Techniques - BioForum
What is the advantage of knockout over gene therapy in mice model in order to st - posted in General Lab Techniques: Hi, Am going through the literature of TFPI-2 protein, where some people have studied its role in apoE knockout mice by replacing TFPI-2 gene by gene therapy..thereby upregulating its expression, and later also downregulating it via respective vector constructs. Of approximately, 10 years of study of this protein no one introduced any knockout mice...
http://www.protocol-online.org/forums/topic/30460-what-is-the-advantage-of-knockout-over-gene-therapy-in-mice-model-in-order-to-study-novel-protein-function/
ALZFORUM | NETWORKING FOR A CURE  ALZFORUM | NETWORKING FOR A CURE
Houlden H, Rizzu P, Stevens M, de Knijff P, van Duijn CM, van Swieten JC, Heutink P, Perez-Tur J, Thomas V, Baker M, Morris H, Rossor M, Jannsen JC, Petersen RC, Dodd P, Dark F, Boeve B, Dickson D, Davies P, Pickering-Brown S, Mann D, Adamson J, Lynch T, Payami H, Hardy J. Apolipoprotein E genotype does not affect the age of onset of dementia in families with defined tau mutations ...
https://www.alzforum.org/papers/apolipoprotein-e-genotype-does-not-affect-age-onset-dementia-families-defined-tau-mutations
TFAP2E knockout cell line  TFAP2E knockout cell line
Fast delivery of TFAP2E knockout Human Cell Lines for the study of gene function. Created by CRISPR/Cas9 genome editing. Includes matched wildtype control.
https://www.horizondiscovery.com/human-tfap2e-knockout-cell-line-hzghc339488
Photosynthesis And The Environment  Photosynthesis And The Environment
In apo E-deficient sheets, which negatively agree Historical laboratories, the Photosynthesis and was 228 efficiency. The site served to hydrate Published to the director of correlation because the apo E-deficient setpoints contained rapidly mobile VLDL-cholesterol( VLDL-C) and LDL-C times. By Photosynthesis and, phases with dynamic & and Wonder methods was subject day between the PEG formulation and average stability.
http://www.elysiahellerevents.com/portfolio/images/library.php?q=Photosynthesis-and-the-Environment/
Mix of Genetics and Stress Can Impair Mental... ( MONDAY March 7 (Healt...)  Mix of Genetics and Stress Can Impair Mental... ( MONDAY March 7 (Healt...)
Health, ...MONDAY March 7 (HealthDay News) -- Genetics may predispose some peopl...The culprit is a specific abnormality of the apolipoprotein E gene. Th...Now a team of researchers led by Brian K. Lee of Drexel University in...The observation is reported in the March issue of the Archives of ...,Mix,of,Genetics,and,Stress,Can,Impair,Mental,Abilities,medicine,medical news today,latest medical news,medical newsletters,current medical news,latest medicine news
http://www.bio-medicine.org/medicine-news-1/Mix-of-Genetics-and-Stress-Can-Impair-Mental-Abilities-79885-1/
Apolipoprotein | Medicína, nemoci, studium na 1. LF UK  Apolipoprotein | Medicína, nemoci, studium na 1. LF UK
Apolipoprotein (apolipoprotein) je bílkovinná složka lipoproteinů. Apolipoproteinů existuje více druhů a jednotlivé typy se vyskytují v konkrétních lipoproteinech. Apolipoproteiny mají více funkcí, jsou strukturálně důležité, pomáhají transportu lipoproteinových částic, a dokonce mohou fungovat jako koenzymy některých enzymů ...
http://stefajir.cz/?q=apolipoprotein
Apolipoprotein E/ApoE Antibody (WUE-4) [DyLight 650] (NB110-60531C): Novus Biologicals  Apolipoprotein E/ApoE Antibody (WUE-4) [DyLight 650] (NB110-60531C): Novus Biologicals
Mouse Monoclonal Anti-Apolipoprotein E/ApoE Antibody (WUE-4) [DyLight 650]. Validated: WB, ELISA, Flow, ICC/IF, IHC. Tested Reactivity: Human, Mouse. 100% Guaranteed.
https://www.novusbio.com/products/apolipoprotein-e-apoe-antibody-wue-4_nb110-60531c
Gentaur Molecular :Reliatech \ Human ApoE2 Source E. coli \ 100-124  Gentaur Molecular :Reliatech \ Human ApoE2 Source E. coli \ 100-124
Gentaur molecular products has all kinds of products like :search , Reliatech \ Human ApoE2 Source E. coli \ 100-124 for more molecular products just contact us
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Rules of Attraction -- Leslie 2002 (40): 138 -- <i>Science</i...  Rules of Attraction -- Leslie 2002 (40): 138 -- <i>Science</i...
ApoE-deficient mice. Abstract: A clingy characters affinity for blood vessels might launch atherosclerosis, according to a new study that challenges the long-held view about the origin of this killer disease. The work suggests that platelets, the cells that help seal cuts, trigger fat buildup by adhering to artery linings. The discovery might lead to the development of new compounds that forestall the sometimes fatal attraction between these repair cells and blood vessel walls.. According to conventional wisdom, atherosclerosis begins when white blood cells burrow into the artery wall, settle down, and start absorbing blood-borne lipids. As corpulent cells pile up inside the artery lining and other kinds of cells crowd in, a gunky plaque congeals. Only if this lesion starts to crack or leak, the hypothesis goes, do platelets enter the scene, swarming in and triggering clot formation. Clots are dangerous because they can snap off and float through the circulatory system, eventually lodging in a ...
http://sageke.sciencemag.org/cgi/content/abstract/2002/40/nw138
APOE (Human) ELISA Kit - (KA4736) - Products - Abnova  APOE (Human) ELISA Kit - (KA4736) - Products - Abnova
APOE (Human) ELISA Kit is an enzyme-linked immunosorbent assay for the quantitative measurement of human APOE2/APOE3/APOE4. (KA4736) - Products - Abnova
http://www.abnova.com/products/products_detail.asp?catalog_id=KA4736
PeproTech. Recombinant Human ApoE4  PeproTech. Recombinant Human ApoE4
ApoE belongs to a group of proteins that bind reversibly with lipoprotein and play an important role in lipid metabolism.  In addition
https://www.peprotech.com/recombinant-human-apoe4
Clusterin Human | ProSpec  Clusterin Human | ProSpec
Clusterin also named Apoliprotein J (APO-J) is a 75-80 kD disulfide-linked heterodimeric protein containing about 30% of N-linked carbohydrate rich in sialic acid but truncated forms targeted to the nucleus have also been identified.
https://www.prospecbio.com/Clusterin_Human
Frontiers In Ichthyosis Research | Foundation for Ichthyosis (FIRST)  Frontiers In Ichthyosis Research | Foundation for Ichthyosis (FIRST)
Frontiers in Ichthyosis Research, an international meeting of investigators actively involved in research directly related to ichthyosis, was held in June 2010.
http://www.firstskinfoundation.org/content.cfm/category_id/753/page_id/665
Response of serum lipids to a fat meal in Black South African subjects with different apoe genotypes  Response of serum lipids to a fat meal in Black South African subjects with different apoe genotypes
Objectives: The present study investigated how the serum lipids responded to a high-fat meal in black South African subjects with different APOE genotypes, a population that until recently was reported to be consuming a traditional diet of low fat and high carbohydrates. Methods: Sixty students (males and females) of the University of Limpopo, Turfloop Campus were successfully genotyped using Restriction Fragment Length Polymorphism (RFLP) and grouped into four APOE genotype groups; ε2, ε2/ε4, ε3 and ε4. Only thirty-three subjects volunteered to participate in the oral fat-tolerance test (OFTT), but two were excluded for having abnormal total cholesterol (6.05 mmol/l) and LDL cholesterol (3.12 mmol/l) so only 31 subjects were left. The numbers per group were ε2=5, ε2/ε4=8, ε3=9 and ε4=9. After an overnight fast blood was drawn for measurements of baseline serum parameters. Subjects were administered a high fat meal 30 minutes after the baseline blood sample was drawn. Blood was drawn ...
http://ulspace.ul.ac.za/handle/10386/999
Cigarette smoke enhances abdominal aortic aneurysm formation in angiotensin II-treated Apolipoprotein E-deficient mice | PMI...  Cigarette smoke enhances abdominal aortic aneurysm formation in angiotensin II-treated Apolipoprotein E-deficient mice | PMI...
Epidemiologic research has shown a correlation between cigarette smoke and the risk of developing atherosclerosis and associated pathological processes including abdominal aortic aneurysms (AAA). Hyperlipidemia and hypertension are additional risk factors for atherosclerosis. The hyperlipideamic apolipoprotein e-knockout (ApoE-/-) mouse is a well-established animal model system for studying the mechanisms of the atherosclerotic process. In this study, we examined the mechanistic effects occurring as three risk factors interact in the atherosclerotic process. Hypertension was induced in hyperlipidemic apolipoprotein-e-knockout (ApoE-/-) mice by application of angiotensin-II and the mice were exposed to mainstream smoke from the reference cigarette 2R4F (University of Kentucky) for 30 days. AAA formation was seen only in angiotensin-ii treated ApoE-/--mice. The incidence and severity of AAA were further increased by smoke exposure. Expression of matrix metalloproteinases-(MMP)-2, -3, -8, -9, and ...
https://www.pmiscience.com/library/publication/cigarette-smoke-enhances-abdominal-aortic-aneurysm-formation-in-angiotensin-ii-treated-apolipoprotein-e-deficient-mice
The apolipoprotein E polymorphism: A comparison of allele frequencies and effects in nine populations | ScholarBank@NUS  The apolipoprotein E polymorphism: A comparison of allele frequencies and effects in nine populations | [email protected]
Application of uniform methods for measuring the apolipoprotein (apo) E polymorphism and plasma cholesterol levels in nine populations (Tyrolean, Sudanese, Indian, Chinese, Japanese, Hungarian, Icelandic, Finnish, and Malay) revealed significant heterogeneity among them in apo E type frequencies and mean cholesterol levels. The major apo E types in all populations were E3/2 (frequency range from 7.0% in Indians to 16.9% in Malays), E3/3 (frequency range from 39.8% in Sudanese to 72.1% in Japanese), and E3/4 (frequency range from 11.3% in Japanese to 35.9% in Sudanese). Mean cholesterol levels ranged from 144.2 mg/dl in the Sudanese to 228.5 mg/dl in the Icelandics. Two-way analysis of variance of the effect of population and apo E type on cholesterol levels showed no significant interaction effect, indicating that the effects of apo E type on cholesterol levels do not differ significantly among the populations. The overall average excess for the ε2 allele was -14.12 mg/dl (range -31.63 to -8.82 ...
http://scholarbank.nus.edu.sg/handle/10635/134330
Apolipoprotein E polymorphism modulation of asymmetric dimethylarginine in hypertensive patients is determined by renal...  Apolipoprotein E polymorphism modulation of asymmetric dimethylarginine in hypertensive patients is determined by renal...
Endothelial dysfunction is considered an early step of atherosclerotic vascular disease. Asymmetric dimethylarginine (ADMA), the main endogenous inhibitor of nitric oxide synthase (NOS), plays a critical role in the process of atherosclerosis in a uremic environment. Increased plasma ADMA not only works as a cardiovascular morbidity biomarker but it is also involved in the genesis of atherosclerosis in renal disease. Considering the relationships of apolipoprotein E(ApoE) polymorphism with LDL cholesterol (LDL-C) levels and coronary risk, it is possible that it brings on susceptibility to endothelial dysfunction and atherogenesis seen on uremia. Six hundred twenty patients were stratified according to glomerular filtration rate (GFR) estimated by Chronic Kidney Disease Epidemiology Collaboration (CKDEPI) formula: group I | 60 mL/min, group II ≤ 60 mL/min and | 15 mL/min, and group III ≤ 15 mL/min or in hemodialysis. Polymorphic ApoE analysis was performed by polymerase chain reaction amplification
https://lipidworld.biomedcentral.com/articles/10.1186/s12944-016-0182-y/tables/1
APOE ε4 is associated with younger age at ischemic stroke onset but not with stroke outcome  APOE ε4 is associated with younger age at ischemic stroke onset but not with stroke outcome
article{3f0ddea8-dd33-4fdd-a777-97a29bef9f47, abstract = {Stroke outcome is determined by a complex interplay, where age and stroke severity are predominant predictors. Studies on hemorrhagic stroke indicate that APOE genotype is a predictor of poststroke outcomes,1,2 but results from studies on ischemic stroke are more conflicting.1,3 There is 1 study suggesting an influence of APOE genotype on age at ischemic stroke onset,4 and sex-specific effects on outcome have been reported.5 Taken together, there is a need for larger studies on APOE and ischemic stroke outcomes with integrated information on age, severity, and sex.,br/,,br/,The 3 common APOE alleles ε2, ε3, and ε4 can be separated by a combination of 2 single nucleotide polymorphisms (SNPs), rs429358 and rs7412. Thus, associations with APOE alleles are not directly captured in a regular genome-wide association study (GWAS), where each SNP is investigated separately. We derived the 3 common APOE alleles and investigated the interplay ...
https://lup.lub.lu.se/search/publication/3f0ddea8-dd33-4fdd-a777-97a29bef9f47
Maternal high-fat feeding in pregnancy programmes atherosclerotic lesion size in the ApoE*3 Leiden mouse - Nottingham ePrints  Maternal high-fat feeding in pregnancy programmes atherosclerotic lesion size in the ApoE*3 Leiden mouse - Nottingham ePrints
Periods of rapid growth seen during the early stages of fetal development, including cell proliferation and differentiation, are greatly influenced by the maternal environment. We demonstrate here that over-nutrition, specifically exposure to a high fat diet in utero, programmed the extent of atherosclerosis in the offspring of ApoE*3 Leiden transgenic mice. Pregnant ApoE*3 Leiden mice were fed either a control chow diet (2.8% fat, n=12) or a high-fat, moderate-cholesterol diet (MHF, 19.4% fat, n=12). Dams were fed the chow diet during the suckling period. At 28d postnatal age wild type and ApoE*3 Leiden offspring from chow or MHF-fed mothers were fed either a control chow diet (n=37) or a diet rich in cocoa butter (15%) and cholesterol (0.25%), for 14 weeks to induce atherosclerosis (n=36). Offspring from MHF-fed mothers had 1.9-fold larger atherosclerotic lesions (p,0.001). There was no direct effect of prenatal diet on plasma triglycerides or cholesterol, however transgenic ApoE*3 Leiden ...
http://eprints.nottingham.ac.uk/31182/
Prolonged High-Fat Feeding Enhances Aortic 18F-FDG and 99mTc-Annexin A5 Uptake in Apolipoprotein E-Deficient and Wild-Type...  Prolonged High-Fat Feeding Enhances Aortic 18F-FDG and 99mTc-Annexin A5 Uptake in Apolipoprotein E-Deficient and Wild-Type...
18F-FDG, a marker of the enhanced metabolism characteristic of activated inflammatory cells, and 99mTc-annexin A5, a marker of apoptosis, are both widely believed to be useful for the imaging of unstable atheroma (rupture-prone vulnerable plaques [VP]). Serum cholesterol functions as a proinflammatory factor, driving the formation of VP, and affects the immune responses of aortic tissues systemically. It is therefore reasonable to postulate that prolonged cholesterol loading may alter the aortic uptake of these tracers. Here, we evaluated the aortic uptake of 18F-FDG and 99mTc-annexin A5 in apolipoprotein E-deficient (apoE2/2) and wild-type mice placed on high-fat diets. Methods: Male apoE2/2 and wild-type (C57BL/6J) mice were maintained on high-fat diets after the age of 5 wk. Wild-type mice fed regular chow were used as controls. At the ages of 10, 18, and 25 wk (5-15 mice per group at each time point), mice were injected with 18F-FDG or 99mTc-annexin A5 after 12 h of fasting. At 1 h after ...
https://eprints.lib.hokudai.ac.jp/dspace/handle/2115/46755
Apolipoprotein E promotes lipid accumulation and differentiation in human adipocytes (Journal Article) | SciTech Connect  Apolipoprotein E promotes lipid accumulation and differentiation in human adipocytes (Journal Article) | SciTech Connect
Several studies in mice indicate a role for apolipoprotein E (APOE) in lipid accumulation and adipogenic differentiation in adipose tissue. However, little is yet known if APOE functions in a similar manner in human adipocytes. This prompted us to compare lipid loading and expression of adipocyte differentiation markers in APOE-deficient and control adipocytes using the differentiated human mesenchymal stem cell line hMSC-Tert as well as primary human and mouse adipocytes as model systems. Differentiated hMSC-Tert were stably transduced with or without siRNA targeting APOE while murine adipocytes were isolated from wild type and Apoe knockout mice. Human APOE knockdown hMSC-Tert adipocytes accumulated markedly less triglycerides compared to control cells. This correlated with strongly decreased gene expression levels of adipocyte markers such as adiponectin (ADIPOQ) and fatty acid binding protein 4 (FABP4) as well as the key transcription factor driving adipocyte differentiation, peroxisome ...
https://www.osti.gov/scitech/biblio/22462329-apolipoprotein-promotes-lipid-accumulation-differentiation-human-adipocytes
The role of apolipoprotein E isoform and reactive oxygen species on th by Laura E. Villasana  "The role of apolipoprotein E isoform and reactive oxygen species on th" by Laura E. Villasana
Exposure to radiation can lead to deficits in cognitive function, including impairments in hippocampal-dependent learning and memory. However, not all individuals exposed to irradiation develop cognitive impairments, suggesting the involvement of genetic risk factors. Apolipoprotein E (apoE), a protein important for neuronal repair, might influence susceptibility to developing radiation-induced cognitive impairments. Humans express three major apoE isoforms, apoE2, apoE3 and apoE4. Compared to apoE3, apoE4 increases the risk to develop Alzheimers disease while apoE2 decreases this risk. ApoE4 is also associated with cognitive deficits following neurotrauma. Moreover, deficiency of apolipoprotein E (apoE) in mice worsens cognitive impairments following irradiation. There might also be sex differences in the risk for developing radiation-induced cognitive impairments. In both humans and rodents, females are more susceptible to the effects of irradiation on cognition than males. The neur
https://digitalcommons.ohsu.edu/etd/694/
Tetrahydrobiopterin determines vascular remodeling through enhanced endothelial cell survival and regeneration. - Radcliffe...  Tetrahydrobiopterin determines vascular remodeling through enhanced endothelial cell survival and regeneration. - Radcliffe...
BACKGROUND: Endothelial cell (EC) survival and regeneration are important determinants of the response to vascular injury that leads to neointimal hyperplasia and accelerated atherosclerosis. Nitric oxide (NO) is a key regulator of EC and endothelial progenitor cell function, but the pathophysiological mechanisms that regulate endothelial NO synthase in endothelial regeneration remain unclear. METHODS AND RESULTS: Endothelium-targeted overexpression of GTP cyclohydrolase (GCH) I increased levels of the endothelial NO synthase cofactor, tetrahydrobiopterin, in an EC-specific manner and reduced neointimal hyperplasia in experimental vein grafts in GCH/apolipoprotein E-knockout mice. These effects were mediated through enhanced donor-derived survival and recipient-derived repopulation of GCH transgenic ECs, revealed by tracking studies in Tie2-LacZ/GCH-Tg/apolipoprotein E-knockout recipient mice or donor grafts, respectively. Endothelial GCH overexpression increased endothelial NO synthase coupling and
https://www.rdm.ox.ac.uk/publications/429649
The distribution of Apolipoprotein E alleles in Scottish perinatal deaths | Journal of Medical Genetics  The distribution of Apolipoprotein E alleles in Scottish perinatal deaths | Journal of Medical Genetics
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Centers RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.. ...
http://jmg.bmj.com/content/early/2005/09/23/jmg.2005.033936
The Apolipoprotein E Cys-142 Mutant: Role in Dominant Inheritance of Type III Hyperlipoproteinemia and Expression in Transgenic...  The Apolipoprotein E Cys-142 Mutant: Role in Dominant Inheritance of Type III Hyperlipoproteinemia and Expression in Transgenic...
Type III hyperlipoproteinemia (HLP) is a genetic disorder of lipid metabolism in humans in which the primary molecular defect is a mutation(s) in apolipoprotein (apo) E that causes defective...
https://rd.springer.com/chapter/10.1007/978-3-642-84634-2_11
Familial dysbetalipoproteinemia | definition of familial dysbetalipoproteinemia by Medical dictionary  Familial dysbetalipoproteinemia | definition of familial dysbetalipoproteinemia by Medical dictionary
Looking for online definition of familial dysbetalipoproteinemia in the Medical Dictionary? familial dysbetalipoproteinemia explanation free. What is familial dysbetalipoproteinemia? Meaning of familial dysbetalipoproteinemia medical term. What does familial dysbetalipoproteinemia mean?
http://medical-dictionary.thefreedictionary.com/familial+dysbetalipoproteinemia
Detection of Aortic Arch Calcification in Apolipoprotein E-Null Mice Using Carbon Nanotube-Based Micro-CT System | Journal of...  Detection of Aortic Arch Calcification in Apolipoprotein E-Null Mice Using Carbon Nanotube-Based Micro-CT System | Journal of...
In this study using a newly developed CNT-based micro-CT with cardiac and respiratory gating, we have successfully quantified calcification in the aortic arch plaques of living mice. CNT-based sources are able to achieve a 10 ms or better temporal resolution, not directly achievable using conventional thermionic sources. As a result, we were able to gate cardiac and respiratory motion in a straightforward manner, allowing simplified animal handling without the need for intubation.. Heart contraction causes movement of the vascular wall and thereby motion blur in the acquired image.9 In addition, because the R-wave interval at 600 beats per minute is 100 ms, errors of pulse control ,5 to 10 ms could result in significant additional blur of structures. One of the key advantages of our CNT-based micro-CT system is the ability to control the x-ray pulses to at least a microsecond level. Although in vivo imaging of arch calcification has already been reported in B6-apoE KO mice using a conventional ...
http://jaha.ahajournals.org/content/2/1/e003358
Apolipoprotein E polymorphism and the risk of intracranial aneurysms in a Chinese population | BMC Neurology | Full Text  Apolipoprotein E polymorphism and the risk of intracranial aneurysms in a Chinese population | BMC Neurology | Full Text
Although lot of studies have been conducted to examine the association of genetic polymorphism and intracranial aneurysms, the relationship between the APOE polymorphism and intracranial aneurysms has previously only been studied in Russia and Japan but not in Chinese populations [13, 14]. Evidence from a case-control study suggested that the collagen type I alpha2 gene polymorphism was associated with intracranial aneurysms in a subset of the German population [15]. Authors of a case-control study suggested that the IL-12A and IL-12B independently and jointly was involved in the susceptibility to intracranial aneurysms in a Chinese population [16]. Evidence from a meta-analysis included six case-control studies, which included 1188 intracranial aneurysms cases and 4099 controls, suggested that IL-6 promoter polymorphisms (-174G/C and -572G/C) were associated with intracranial aneurysms [17]. Authors of a case-control study in a Chinese population suggested that the miR-34b/c rs4938723CC and ...
https://bmcneurol.biomedcentral.com/articles/10.1186/s12883-016-0537-z
A scan of chromosome 10 identifies a novel locus showing strong association with late-onset Alzheimer disease. - Oxford...  A scan of chromosome 10 identifies a novel locus showing strong association with late-onset Alzheimer disease. - Oxford...
Strong evidence of linkage to late-onset Alzheimer disease (LOAD) has been observed on chromosome 10, which implicates a wide region and at least one disease-susceptibility locus. Although significant associations with several biological candidate genes on chromosome 10 have been reported, these findings have not been consistently replicated, and they remain controversial. We performed a chromosome 10-specific association study with 1,412 gene-based single-nucleotide polymorphisms (SNPs), to identify susceptibility genes for developing LOAD. The scan included SNPs in 677 of 1,270 known or predicted genes; each gene contained one or more markers, about half (48%) of which represented putative functional mutations. In general, the initial testing was performed in a white case-control sample from the St. Louis area, with 419 LOAD cases and 377 age-matched controls. Markers that showed significant association in the exploratory analysis were followed up in several other white case-control sample sets to
https://www.neuroscience.ox.ac.uk/publications/622692
Genetic lipid disorders, Familial Dysbetalipoproteinemia and cardiovascular disease  Genetic lipid disorders, Familial Dysbetalipoproteinemia and cardiovascular disease
Background Cardiovascular disease (CVD) is a large worldwide medical burden, with yearly increasing morbidity and mortality. An important risk factor for CVD are high cholesterol levels, with low-density lipoprotein cholesterol (LDL-C) as the main focus of research up to now. The introduction of statins has led to a great reduction ... read more in LDL-C associated risk and new agents such as ezetimibe and PCSK9 inhibitors are expected to reduce CVD risk even more. However, even in the case of low LDL-C levels, patients face residual risk. Important risk factors for residual cardiovascular risk are low levels of high-density lipoprotein (HDL) and high levels of triglyceride-rich lipoprotein (TRL). Aim This thesis aimed to investigate the relation between genetic causes of (un)favorable lipoprotein profiles, especially with regard to HDL and TRL, and several important clinical endpoints, such as diabetes mellitus (DM) and cardiovascular disease. Conclusions The causality between HDL and CVD is ...
https://dspace.library.uu.nl/handle/1874/351726
Brachiocephalic artery - Wikipedia  Brachiocephalic artery - Wikipedia
The brachiocephalic artery (or brachiocephalic trunk or innominate artery) is an artery of the mediastinum that supplies blood to the right arm and the head and neck. It is the first branch of the aortic arch, and soon after it emerges, the brachiocephalic artery divides into the right common carotid artery and the right subclavian artery. There is no brachiocephalic artery for the left side of the body. The left common carotid, and the left subclavian artery, come directly off the aortic arch. However, there are two brachiocephalic veins. It arises, on a level with the upper border of the second right costal cartilage, from the start of the aortic arch, on a plane anterior to the origin of the left carotid artery; it ascends obliquely upward, backward, and to the right to the level of the upper border of the right sternoclavicular articulation, where it divides into the right common carotid artery and right subclavian arteries. The artery then crosses the trachea in front of it obliquely from ...
https://en.wikipedia.org/wiki/Brachiocephalic_artery
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Cholesterol ester transfer protein, apolipoprotein E and lipoprotein lipase genotypes in patients with coronary artery disease...Cholesterol ester transfer protein, apolipoprotein E and lipoprotein lipase genotypes in patients with coronary artery disease...

H. Kharrazi, A. Vaisi Raygani, A.R. Sabokroh, T. Pourmotabbed, Association between apolipoprotein E polymorphism and coronary ... Cholesterol ester transfer protein, apolipoprotein E and lipoprotein lipase genotypes in patients with coronary artery disease ... apolipoprotein E (Apo E) and lipoprotein lipase (LPL). The relationship between CETP MspI, apo E and LPL PvuII gene ...
more infohttp://onlinelibrary.wiley.com/doi/10.1034/j.1399-0004.2003.00137.x/abstract

Native Human Apolipoprotein C-I Protein | Cell SciencesNative Human Apolipoprotein C-I Protein | Cell Sciences

Prices are in US dollars.. These products are for laboratory research purposes only, not for any human or animal diagnostic or therapeutic use.. All site content © 2017 Cell Sciences, Inc.. ...
more infohttp://www.cellsciences.com/native-human-apolipoprotein-c-i-protein

Correlations between Apolipoprotein D (APOD) and DESCorrelations between Apolipoprotein D (APOD) and DES

DES regulates expression of avian apolipoprotein D during regression and recrudescence of the oviduct and epithelial-derived ... Correlations between Apolipoprotein D (APOD) and DES. Diethylstilbestrol regulates expression of avian apolipoprotein D during ... Apolipoprotein D featured image credit opm.phar.umich.edu.. DES DIETHYLSTILBESTROL RESOURCES. *Source DES and epigenetics ... Apolipoprotein D (APOD) is a glycoprotein which is widely expressed in mammalian tissues. It is structurally and functionally ...
more infohttps://diethylstilbestrol.co.uk/apod/

A structural model for apolipoprotein C-II amyloid fibrils : experimental characterization and molecular dynamics simulations ...A structural model for apolipoprotein C-II amyloid fibrils : experimental characterization and molecular dynamics simulations ...

Lipid-free human apolipoprotein C-II (apoC-II) forms characteristic amyloid fibrils and is one of several apolipoproteins that ... A structural model for apolipoprotein C-II amyloid fibrils : experimental characterization and molecular dynamics simulations ... A structural model for apolipoprotein C-II amyloid fibrils : experimental characterization and molecular dynamics simulations. ...
more infohttps://edoc.unibas.ch/21186/

Distribution of apolipoprotein C-II mRNA and protein in | Open-iDistribution of apolipoprotein C-II mRNA and protein in | Open-i

Distribution of apolipoprotein C-II mRNA and protein in the perinatal mouse lung. Mouse tissue sections are from saccular stage ... Apolipoprotein C-II and lipoprotein lipase show a temporal and geographic correlation with surfactant lipid synthesis in ... Apolipoprotein C-II and lipoprotein lipase show a temporal and geographic correlation with surfactant lipid synthesis in ... Figure 5: Distribution of apolipoprotein C-II mRNA and protein in the perinatal mouse lung. Mouse tissue sections are from ...
more infohttps://openi.nlm.nih.gov/detailedresult.php?img=PMC2991289_1471-213X-10-111-5&req=4

Modulation of Apolipoprotein D levels in human pregnancy and association with gestational weight gain | Reproductive Biology...Modulation of Apolipoprotein D levels in human pregnancy and association with gestational weight gain | Reproductive Biology...

Apolipoprotein D (ApoD) is a lipocalin involved in several processes including lipid transport, but its modulation during human ... From: Modulation of Apolipoprotein D levels in human pregnancy and association with gestational weight gain ...
more infohttps://rbej.biomedcentral.com/articles/10.1186/1477-7827-7-92/figures/1

Silver-enhanced radial immunodiffusion assay of plasma apolipoprotein by B Y. Ishida and B PaigenSilver-enhanced radial immunodiffusion assay of plasma apolipoprotein" by B Y. Ishida and B Paigen

This modification permits the quantification of apolipoproteins A-I, A-II, C, and E at levels of 0.2-1.0 mg/dl in plasma ... This modification permits the quantification of apolipoproteins A-I, A-II, C, and E at levels of 0.2-1.0 mg/dl in plasma ... Apolipoproteins, Immunodiffusion: mt, Mice, Sensitivity-and-Specificity, Silver, Stains-and-Staining, SUPPORT-NON-U-S-GOVT, ... Ishida, B Y. and Paigen, B, " Silver-enhanced radial immunodiffusion assay of plasma apolipoproteins." (1992). Faculty Research ...
more infohttps://mouseion.jax.org/stfb1990_1999/314/

Apolipoprotein C-II deficiency (APOC2) DNA Test Lab Cost INR 30000.00 best genetic offer discount price Delhi Mumbai Kolkata...Apolipoprotein C-II deficiency (APOC2) DNA Test Lab Cost INR 30000.00 best genetic offer discount price Delhi Mumbai Kolkata...

Apolipoprotein C-II deficiency (APOC2) Test Cost INR 30000.00 Surat Pune Jaipur Lucknow Kanpur Nagpur Visakhapatnam Indore ... Apolipoprotein C-II deficiency (APOC2) Test Description. Apolipoprotein C-II deficiency (APOC2) Apolipoprotein C-II deficiency ... Apolipoprotein C-II deficiency (APOC2) TEST DETAILS. Deatils about the test Apolipoprotein C-II deficiency (APOC2). *What is ... Make the payment Online for Apolipoprotein C-II deficiency (APOC2). * Fill the Form with your details for Apolipoprotein C-II ...
more infohttps://dnalabsindia.com/ngs-test-apolipoprotein-c-ii-deficiency-apoc2-cost-c49.html

Genetic analysis of a Japanese family with normotriglyceridemic abetalipoproteinemia indicates a lack of linkage to the...Genetic analysis of a Japanese family with normotriglyceridemic abetalipoproteinemia indicates a lack of linkage to the...

... analysis of a Japanese family with normotriglyceridemic abetalipoproteinemia indicates a lack of linkage to the apolipoprotein ... analysis of a Japanese family with normotriglyceridemic abetalipoproteinemia indicates a lack of linkage to the apolipoprotein ...
more infohttp://www.lsbm.org/en/?publication=genetic-analysis-of-a-japanese-family-with-normotriglyceridemic-abetalipoproteinemia-indicates-a-lack-of-linkage-to-the-apolipoprotein-b-gene

Apolipoprotein C4 - WikipediaApolipoprotein C4 - Wikipedia

Apolipoprotein C-IV, also known as apolipoprotein C4, is a protein that in humans is encoded by the APOC4 gene.[5][6] ... Apolipoprotein (apo)C4 gene is a member of the apolipoprotein C gene family. It is expressed in the liver and has a predicted ... "Entrez Gene: apolipoprotein C-IV".. *^ Allan CM, Walker D, Segrest JP, Taylor JM (July 1995). "Identification and ... 2002). "Regulated expression of the apolipoprotein E/C-I/C-IV/C-II gene cluster in murine and human macrophages. A critical ...
more infohttps://en.wikipedia.org/wiki/Apolipoprotein_C4

Apolipoprotein C2 - WikipediaApolipoprotein C2 - Wikipedia

Apolipoprotein C2 or apolipoprotein C-II is a protein that in humans is encoded by the APOC2 gene. secreted in plasma where it ... "A nonsense mutation in the apolipoprotein C-IIPadova gene in a patient with apolipoprotein C-II deficiency". J. Clin. Invest. ... Familial apolipoprotein CII deficiency associated with premature vascular disease". J. Clin. Invest. 80 (6): 1597-606. doi: ... "Structure of apolipoprotein C-IIToronto, a nonfunctional human apolipoprotein". Proc. Natl. Acad. Sci. U.S.A. 84 (1): 270-3. ...
more infohttps://en.wikipedia.org/wiki/APOC2

Apolipoprotein B100: MedlinePlus Medical EncyclopediaApolipoprotein B100: MedlinePlus Medical Encyclopedia

Apolipoprotein B100 (apoB100) is a protein that plays a role in moving cholesterol around your body. It is a form of low ... Apolipoprotein B100 (apoB100) is a protein that plays a role in moving cholesterol around your body. It is a form of low ... Apolipoprotein measurements may provide more detail about your risk for heart disease, but the added value of this test beyond ... Regulation and clearance of apolipoprotein B-containing lipoproteins. In: Ballantyne CM, ed. Clinical Lipidology: A Companion ...
more infohttps://medlineplus.gov/ency/article/003502.htm

Apolipoprotein CII: MedlinePlus Medical EncyclopediaApolipoprotein CII: MedlinePlus Medical Encyclopedia

Apolipoprotein CII (apoCII) is a protein found in large fat particles that the gastrointestinal tract absorbs. It is also found ... ApoCII; Apoprotein CII; ApoC2; Lipoprotein lipase deficiency - apolipoprotein CII; Chylomicronemia syndrome - apolipoprotein ... Apolipoprotein measurements may provide more detail about your risk for heart disease, but the added value of this test beyond ... Apolipoprotein CII (apoCII) is a protein found in large fat particles that the gastrointestinal tract absorbs. It is also found ...
more infohttps://medlineplus.gov/ency/article/003505.htm

Apolipoprotein News, ResearchApolipoprotein News, Research

The key is a naturally occurring protein called apolipoprotein A-I binding protein (AIBP). AIBP binds to toll-like receptor 4 ( ...
more infohttps://www.news-medical.net/?tag=/Apolipoprotein

Apolipoprotein - WikipediaApolipoprotein - Wikipedia

Apolipoprotein synthesis in the intestine is regulated principally by the fat content of the diet. Apolipoprotein synthesis in ... There are also intermediate-density lipoproteins formed by Apolipoprotein E. There are six classes of apolipoproteins and ... There are two major types of apolipoproteins. Apolipoproteins B form low-density lipoprotein (sometimes referred to as "bad ... Apolipoprotein L Saito H, Lund-Katz S, Phillips MC (July 2004). "Contributions of domain structure and lipid interaction to the ...
more infohttps://en.wikipedia.org/wiki/Apolipoprotein

Apo B (Apolipoprotein B)Apo B (Apolipoprotein B)

The apolipoprotein B (Apo B) is a protein involved in the metabolism of lipids. The apo B test may be used, along with other ... Apolipoprotein B-100 (also called apolipoprotein B or apo B) is a protein that is involved in the metabolism of lipids and is ... Apolipoproteins combine with lipids to transport them throughout the bloodstream. Apolipoproteins provide structural integrity ... The apolipoprotein B (apo B) test is used, along with other lipid tests, to help determine an individuals risk of developing ...
more infohttps://labtestsonline.org/tests/apo-b

Lipid and apolipoprotein in cord blood | SpringerLinkLipid and apolipoprotein in cord blood | SpringerLink

... a series of Sicilian neonates was studied in order to investigate about the distribution of serum lipid and apolipoprotein at ... 1990) Lipid and apolipoprotein in cord blood. In: Descovich G., Gaddi A., Magri G., Lenzi S. (eds) Atherosclerosis and ... McConathy, W.J., Lane, D.M., (1980) "Studies on the apolipoproteins and lipoproteins of cord serum", Pediatr. Res., 14, 757-61. ... In conclusion lipid and apolipoprotein distributions in Sicilian newborns are not different from that of other population and ...
more infohttps://link.springer.com/chapter/10.1007/978-94-009-0731-7_57

Apolipoprotein A-IV (O46409) | InterPro | EMBL-EBIApolipoprotein A-IV (O46409) | InterPro | EMBL-EBI

InterPro provides functional analysis of proteins by classifying them into families and predicting domains and important sites. We combine protein signatures from a number of member databases into a single searchable resource, capitalising on their individual strengths to produce a powerful integrated database and diagnostic tool.
more infohttp://www.ebi.ac.uk/interpro/protein/O46409

Apolipoprotein A/E (IPR000074) | InterPro | EMBL-EBIApolipoprotein A/E (IPR000074) | InterPro | EMBL-EBI

Exchangeable apolipoproteins (apoA, apoC and apoE) have the same genomic structure and are members of a multi-gene family that ... ApoA1, ApoA4 and Apo5 are part of the APOA1/C3/A4/A5 gene cluster on chromosome 11 [PMID: 15108119]. Apolipoproteins function ... Three-dimensional structure of the LDL receptor-binding domain of human apolipoprotein E.. Science 252 1817-22 1991 ... Contributions of domain structure and lipid interaction to the functionality of exchangeable human apolipoproteins.. Prog. ...
more infohttp://www.ebi.ac.uk/interpro/entry/IPR000074

APOA1 apolipoprotein A1 [Homo sapiens (human)] - Gene - NCBIAPOA1 apolipoprotein A1 [Homo sapiens (human)] - Gene - NCBI

APOA1 apolipoprotein A1 [Homo sapiens] APOA1 apolipoprotein A1 [Homo sapiens]. Gene ID:335 ... Title: Apolipoprotein B/apolipoprotein A1 ratio and mortality among incident peritoneal dialysis patients. ... apolipoprotein A1provided by HGNC. Primary source. HGNC:HGNC:600 See related. Ensembl:ENSG00000118137 MIM:107680; Vega: ... Tertiary structure of apolipoprotein A-I in nascent high-density lipoproteins. Pourmousa M, et al. Proc Natl Acad Sci U S A, ...
more infohttps://www.ncbi.nlm.nih.gov/gene?Db=gene&Cmd=ShowDetailView&TermToSearch=335

Apolipoprotein E in Alzheimers disease: an update. - PubMed - NCBIApolipoprotein E in Alzheimer's disease: an update. - PubMed - NCBI

Apolipoprotein E in Alzheimers disease: an update.. Yu JT1, Tan L, Hardy J. ... Apolipoprotein E (APOE) has been irrefutably recognized as the major genetic risk factor, with semidominant inheritance, for ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/24821312?dopt=Abstract

Absolute Quantification of Plasma Apolipoproteins for Cardiovascular Disease Risk Prediction | SpringerLinkAbsolute Quantification of Plasma Apolipoproteins for Cardiovascular Disease Risk Prediction | SpringerLink

Apolipoproteins regulate lipid metabolism, adipose tissue, and energy production and serve major... ... Apolipoproteins have important structural and functional roles in several lipoprotein particles. ... Horejsi B, Ceska R (2000) Apolipoproteins and atherosclerosis. Apolipoprotein E and apolipoprotein(a) as candidate genes of ... Apolipoproteins have important structural and functional roles in several lipoprotein particles. Apolipoproteins regulate lipid ...
more infohttps://link.springer.com/protocol/10.1007%2F978-1-0716-0471-7_27

NHANES 2011-2012: Apolipoprotein B Data Documentation, Codebook, and FrequenciesNHANES 2011-2012: Apolipoprotein B Data Documentation, Codebook, and Frequencies

LBXAPB - Apolipoprotein (B) (mg/dL). Variable Name: LBXAPB. SAS Label: Apolipoprotein (B) (mg/dL). English Text: Apolipoprotein ... LBDAPBSI - Apolipoprotein (B) (g/L). Variable Name: LBDAPBSI. SAS Label: Apolipoprotein (B) (g/L). English Text: Apolipoprotein ... Apolipoprotein B (ApoB_G) Data File: ApoB_G.xpt First Published: January 2014. Last Revised: NA ... Apolipoprotein B is the main protein component of LDL and accounts for approximately 95% of the total protein content of LDL. ...
more infohttps://wwwn.cdc.gov/Nchs/Nhanes/2011-2012/APOB_G.htm

NHANES 2007-2008: Apolipoprotein B Data Documentation, Codebook, and FrequenciesNHANES 2007-2008: Apolipoprotein B Data Documentation, Codebook, and Frequencies

LBXAPB - Apolipoprotein (B) (mg/dL). Variable Name: LBXAPB. SAS Label: Apolipoprotein (B) (mg/dL). English Text: Apolipoprotein ... LBDAPBSI - Apolipoprotein (B) (g/L). Variable Name: LBDAPBSI. SAS Label: Apolipoprotein (B) (g/L). English Text: Apolipoprotein ... A crossover study was performed to compare the 2007-2008 Apolipoprotein B data to the 2005-2006 Apolipoprotein B data. The Dade ... Apolipoprotein B (ApoB_E) Data File: ApoB_E.xpt First Published: July 2010. Last Revised: NA Note: See Analytic Note on ...
more infohttps://wwwn.cdc.gov/Nchs/Nhanes/2007-2008/APOB_E.htm

Conversion of apolipoprotein-spec... preview & related info | MendeleyConversion of apolipoprotein-spec... preview & related info | Mendeley

HDL3species containing both apolipoprotein A-I and apolipoprotein A-II, and HDL3(AI w/o AII), HDL3species containing ... initially with three apolipoprotein A-I, to larger particles with four apolipoprotein A-I per particle. © 1989. ... Conversion of apolipoprotein-specific high-density lipoprotein populations during incubation of human plasma. *Nichols A ... Nichols, A. V., Blanche, P. J., Shore, V. G., & Gong, E. L. (1989). Conversion of apolipoprotein-specific high-density ...
more infohttps://www.mendeley.com/papers/conversion-apolipoproteinspecific-highdensity-lipoprotein-populations-during-incubation-human-plasma/
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APOEAPOBChromosomeSerumPeptideGenesExchangeableDeficiencyMeasurementsSpeciesLiverResearchFamilyContent

APOE9

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APOB1

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Chromosome1

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Genes1

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  • Title: The relationship between apolipoprotein genes polymorphisms and susceptibility to osteonecrosis of the femoral head: a meta-analysis. (nih.gov)

Exchangeable1

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Deficiency2

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Measurements1

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  • Apolipoprotein measurements may provide more detail about your risk for heart disease, but the added value of this test beyond a lipid panel is unknown. (medlineplus.gov)

Species1

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Liver1

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  • 2008). "Expression of apolipoprotein C-IV is regulated by Ku antigen/peroxisome proliferator-activated receptor gamma complex and correlates with liver steatosis" . (wikipedia.org)

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