The new and thickened layer of scar tissue that forms on a PROSTHESIS, or as a result of vessel injury especially following ANGIOPLASTY or stent placement.
The innermost layer of an artery or vein, made up of one layer of endothelial cells and supported by an internal elastic lamina.
Damages to the CAROTID ARTERIES caused either by blunt force or penetrating trauma, such as CRANIOCEREBRAL TRAUMA; THORACIC INJURIES; and NECK INJURIES. Damaged carotid arteries can lead to CAROTID ARTERY THROMBOSIS; CAROTID-CAVERNOUS SINUS FISTULA; pseudoaneurysm formation; and INTERNAL CAROTID ARTERY DISSECTION. (From Am J Forensic Med Pathol 1997, 18:251; J Trauma 1994, 37:473)
An increase in the number of cells in a tissue or organ without tumor formation. It differs from HYPERTROPHY, which is an increase in bulk without an increase in the number of cells.
The nonstriated involuntary muscle tissue of blood vessels.
Either of the two principal arteries on both sides of the neck that supply blood to the head and neck; each divides into two branches, the internal carotid artery and the external carotid artery.
Use or insertion of a tubular device into a duct, blood vessel, hollow organ, or body cavity for injecting or withdrawing fluids for diagnostic or therapeutic purposes. It differs from INTUBATION in that the tube here is used to restore or maintain patency in obstructions.
Use of a balloon catheter for dilation of an occluded artery. It is used in treatment of arterial occlusive diseases, including renal artery stenosis and arterial occlusions in the leg. For the specific technique of BALLOON DILATION in coronary arteries, ANGIOPLASTY, BALLOON, CORONARY is available.
Non-striated, elongated, spindle-shaped cells found lining the digestive tract, uterus, and blood vessels. They are derived from specialized myoblasts (MYOBLASTS, SMOOTH MUSCLE).
Injuries to blood vessels caused by laceration, contusion, puncture, or crush and other types of injuries. Symptoms vary by site and mode of injuries and may include bleeding, bruising, swelling, pain, and numbness. It does not include injuries secondary to pathologic function or diseases such as ATHEROSCLEROSIS.
The main artery of the thigh, a continuation of the external iliac artery.
The two principal arteries supplying the structures of the head and neck. They ascend in the neck, one on each side, and at the level of the upper border of the thyroid cartilage, each divides into two branches, the external (CAROTID ARTERY, EXTERNAL) and internal (CAROTID ARTERY, INTERNAL) carotid arteries.
The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell.
Endoscopic examination, therapy or surgery performed on the interior of blood vessels.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
The veins and arteries of the HEART.
The middle layer of blood vessel walls, composed principally of thin, cylindrical, smooth muscle cells and elastic tissue. It accounts for the bulk of the wall of most arteries. The smooth muscle cells are arranged in circular layers around the vessel, and the thickness of the coat varies with the size of the vessel.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
Either of two large arteries originating from the abdominal aorta; they supply blood to the pelvis, abdominal wall and legs.
High energy POSITRONS or ELECTRONS ejected from a disintegrating atomic nucleus.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.
Veins in the neck which drain the brain, face, and neck into the brachiocephalic or subclavian veins.
Recurrent narrowing or constriction of a coronary artery following surgical procedures performed to alleviate a prior obstruction.
Non-human animals, selected because of specific characteristics, for use in experimental research, teaching, or testing.
Surgical insertion of BLOOD VESSEL PROSTHESES, or transplanted BLOOD VESSELS, or other biological material to repair injured or diseased blood vessels.
The vessels carrying blood away from the heart.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
The main trunk of the systemic arteries.
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.
Mitogenic peptide growth hormone carried in the alpha-granules of platelets. It is released when platelets adhere to traumatized tissues. Connective tissue cells near the traumatized region respond by initiating the process of replication.
Devices that provide support for tubular structures that are being anastomosed or for body cavities during skin grafting.
A family of non-enveloped viruses infecting mammals (MASTADENOVIRUS) and birds (AVIADENOVIRUS) or both (ATADENOVIRUS). Infections may be asymptomatic or result in a variety of diseases.
Obstruction of flow in biological or prosthetic vascular grafts.
The condition of an anatomical structure's being constricted beyond normal dimensions.
Cellular DNA-binding proteins encoded by the sis gene (GENES, SIS). c-sis proteins make up the B chain of PLATELET-DERIVED GROWTH FACTOR. Overexpression of c-sis causes tumorigenesis.
Restoration of integrity to traumatized tissue.
The introduction of functional (usually cloned) GENES into cells. A variety of techniques and naturally occurring processes are used for the gene transfer such as cell hybridization, LIPOSOMES or microcell-mediated gene transfer, ELECTROPORATION, chromosome-mediated gene transfer, TRANSFECTION, and GENETIC TRANSDUCTION. Gene transfer may result in genetically transformed cells and individual organisms.
Homopolymer of tetrafluoroethylene. Nonflammable, tough, inert plastic tubing or sheeting; used to line vessels, insulate, protect or lubricate apparatus; also as filter, coating for surgical implants or as prosthetic material. Synonyms: Fluoroflex; Fluoroplast; Ftoroplast; Halon; Polyfene; PTFE; Tetron.
Any of various animals that constitute the family Suidae and comprise stout-bodied, short-legged omnivorous mammals with thick skin, usually covered with coarse bristles, a rather long mobile snout, and small tail. Included are the genera Babyrousa, Phacochoerus (wart hogs), and Sus, the latter containing the domestic pig (see SUS SCROFA).
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
Narrowing or stricture of any part of the CAROTID ARTERIES, most often due to atherosclerotic plaque formation. Ulcerations may form in atherosclerotic plaques and induce THROMBUS formation. Platelet or cholesterol emboli may arise from stenotic carotid lesions and induce a TRANSIENT ISCHEMIC ATTACK; CEREBROVASCULAR ACCIDENT; or temporary blindness (AMAUROSIS FUGAX). (From Adams et al., Principles of Neurology, 6th ed, pp 822-3)
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Elements of limited time intervals, contributing to particular results or situations.
Formation and development of a thrombus or blood clot in the blood vessel.
Pathological conditions involving the CAROTID ARTERIES, including the common, internal, and external carotid arteries. ATHEROSCLEROSIS and TRAUMA are relatively frequent causes of carotid artery pathology.
Pathological processes which result in the partial or complete obstruction of ARTERIES. They are characterized by greatly reduced or absence of blood flow through these vessels. They are also known as arterial insufficiency.
The inferior and superior venae cavae.
The vein which drains the foot and leg.
A genus of brown-rot fungi in the family Coriolaceae. The biologically active ingredients of its species have potential pharmaceutical value.
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.
The portion of the descending aorta proceeding from the arch of the aorta and extending to the DIAPHRAGM, eventually connecting to the ABDOMINAL AORTA.
Application of a ligature to tie a vessel or strangulate a part.
The aorta from the DIAPHRAGM to the bifurcation into the right and left common iliac arteries.
Stents that are covered with materials that are embedded with chemicals that are gradually released into the surrounding milieu.
Device constructed of either synthetic or biological material that is used for the repair of injured or diseased blood vessels.
A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.
Genetically developed small pigs for use in biomedical research. There are several strains - Yucatan miniature, Sinclair miniature, and Minnesota miniature.
Dilation of an occluded coronary artery (or arteries) by means of a balloon catheter to restore myocardial blood supply.
INFLAMMATION of any ARTERIES.
A salt-soluble precursor of elastin. Lysyl oxidase is instrumental in converting it to elastin in connective tissue.
Injuries caused by electric currents. The concept excludes electric burns (BURNS, ELECTRIC), but includes accidental electrocution and electric shock.
A macrolide compound obtained from Streptomyces hygroscopicus that acts by selectively blocking the transcriptional activation of cytokines thereby inhibiting cytokine production. It is bioactive only when bound to IMMUNOPHILINS. Sirolimus is a potent immunosuppressant and possesses both antifungal and antineoplastic properties.
The vessels carrying blood away from the capillary beds.
Agents that affect the rate or intensity of cardiac contraction, blood vessel diameter, or blood volume.
Techniques and strategies which include the use of coding sequences and other conventional or radical means to transform or modify cells for the purpose of treating or reversing disease conditions.
A PDGF receptor that binds specifically to the PDGF-B chain. It contains a protein-tyrosine kinase activity that is involved in SIGNAL TRANSDUCTION.
The return of a sign, symptom, or disease after a remission.
DNA molecules capable of autonomous replication within a host cell and into which other DNA sequences can be inserted and thus amplified. Many are derived from PLASMIDS; BACTERIOPHAGES; or VIRUSES. They are used for transporting foreign genes into recipient cells. Genetic vectors possess a functional replicator site and contain GENETIC MARKERS to facilitate their selective recognition.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
Unstable isotopes of gold that decay or disintegrate emitting radiation. Au 185-196, 198-201, and 203 are radioactive gold isotopes.
Pathological processes involving any of the BLOOD VESSELS in the cardiac or peripheral circulation. They include diseases of ARTERIES; VEINS; and rest of the vasculature system in the body.
Precursor cells destined to differentiate into smooth muscle myocytes (MYOCYTES, SMOOTH MUSCLE).
Nuclear antigen with a role in DNA synthesis, DNA repair, and cell cycle progression. PCNA is required for the coordinated synthesis of both leading and lagging strands at the replication fork during DNA replication. PCNA expression correlates with the proliferation activity of several malignant and non-malignant cell types.
Pathological processes involving the integrity of blood circulation. Hemostasis depends on the integrity of BLOOD VESSELS, blood fluidity, and BLOOD COAGULATION. Majority of the hemostatic disorders are caused by disruption of the normal interaction between the VASCULAR ENDOTHELIUM, the plasma proteins (including BLOOD COAGULATION FACTORS), and PLATELETS.
Any of the tubular vessels conveying the blood (arteries, arterioles, capillaries, venules, and veins).
Small containers or pellets of a solid drug implanted in the body to achieve sustained release of the drug.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
Highly specialized EPITHELIAL CELLS that line the HEART; BLOOD VESSELS; and lymph vessels, forming the ENDOTHELIUM. They are polygonal in shape and joined together by TIGHT JUNCTIONS. The tight junctions allow for variable permeability to specific macromolecules that are transported across the endothelial layer.
Biocompatible materials usually used in dental and bone implants that enhance biologic fixation, thereby increasing the bond strength between the coated material and bone, and minimize possible biological effects that may result from the implant itself.
Tissue that supports and binds other tissues. It consists of CONNECTIVE TISSUE CELLS embedded in a large amount of EXTRACELLULAR MATRIX.
Chronic inflammation and granuloma formation around irritating foreign bodies.
Benzoic acids, salts, or esters that contain an amino group attached to carbon number 2 or 6 of the benzene ring structure.
The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
The use of ultrasound to guide minimally invasive surgical procedures such as needle ASPIRATION BIOPSY; DRAINAGE; etc. Its widest application is intravascular ultrasound imaging but it is useful also in urology and intra-abdominal conditions.
A sensory branch of the MANDIBULAR NERVE, which is part of the trigeminal (5th cranial) nerve. The lingual nerve carries general afferent fibers from the anterior two-thirds of the tongue, the floor of the mouth, and the mandibular gingivae.
Pathological outpouching or sac-like dilatation in the wall of any blood vessel (ARTERIES or VEINS) or the heart (HEART ANEURYSM). It indicates a thin and weakened area in the wall which may later rupture. Aneurysms are classified by location, etiology, or other characteristics.
The deformation and flow behavior of BLOOD and its elements i.e., PLASMA; ERYTHROCYTES; WHITE BLOOD CELLS; and BLOOD PLATELETS.
The fruiting 'heads' or 'caps' of FUNGI, which as a food item are familiarly known as MUSHROOMS, that contain the FUNGAL SPORES.
A member of the family of tissue inhibitor of metalloproteinases. Mutations of the gene for TIMP3 PROTEIN causes Sorsby fundus dystrophy.
A negatively-charged extracellular matrix protein that plays a role in the regulation of BONE metabolism and a variety of other biological functions. Cell signaling by osteopontin may occur through a cell adhesion sequence that recognizes INTEGRIN ALPHA-V BETA-3.
The plan and delineation of prostheses in general or a specific prosthesis.
Filamentous proteins that are the main constituent of the thin filaments of muscle fibers. The filaments (known also as filamentous or F-actin) can be dissociated into their globular subunits; each subunit is composed of a single polypeptide 375 amino acids long. This is known as globular or G-actin. In conjunction with MYOSINS, actin is responsible for the contraction and relaxation of muscle.
A meshwork-like substance found within the extracellular space and in association with the basement membrane of the cell surface. It promotes cellular proliferation and provides a supporting structure to which cells or cell lysates in culture dishes adhere.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
A condition with abnormally high levels of CHOLESTEROL in the blood. It is defined as a cholesterol value exceeding the 95th percentile for the population.
An imaging method using LASERS that is used for mapping subsurface structure. When a reflective site in the sample is at the same optical path length (coherence) as the reference mirror, the detector observes interference fringes.
An octapeptide that is a potent but labile vasoconstrictor. It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME. The amino acid in position 5 varies in different species. To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS.
HYALURONAN-containing proteoglycans found in the EXTRACELLULAR MATRIX of a variety of tissues and organs. Several versican isoforms exist due to multiple ALTERNATIVE SPLICING of the versican MESSENGER RNA.
A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
An endopeptidase that is structurally similar to MATRIX METALLOPROTEINASE 2. It degrades GELATIN types I and V; COLLAGEN TYPE IV; and COLLAGEN TYPE V.
A collective term for interstitial, intracavity, and surface radiotherapy. It uses small sealed or partly-sealed sources that may be placed on or near the body surface or within a natural body cavity or implanted directly into the tissues.
A nucleoside that substitutes for thymidine in DNA and thus acts as an antimetabolite. It causes breaks in chromosomes and has been proposed as an antiviral and antineoplastic agent. It has been given orphan drug status for use in the treatment of primary brain tumors.
The transfer of bacterial DNA by phages from an infected bacterium to another bacterium. This also refers to the transfer of genes into eukaryotic cells by viruses. This naturally occurring process is routinely employed as a GENE TRANSFER TECHNIQUE.
Surgical union or shunt between ducts, tubes or vessels. It may be end-to-end, end-to-side, side-to-end, or side-to-side.
Mice bearing mutant genes which are phenotypically expressed in the animals.
Inflammation of any one of the blood vessels, including the ARTERIES; VEINS; and rest of the vasculature system in the body.
A purely physical condition which exists within any material because of strain or deformation by external forces or by non-uniform thermal expansion; expressed quantitatively in units of force per unit area.
A technique for maintenance or growth of animal organs in vitro. It refers to three-dimensional cultures of undisaggregated tissue retaining some or all of the histological features of the tissue in vivo. (Freshney, Culture of Animal Cells, 3d ed, p1)
White blood cells. These include granular leukocytes (BASOPHILS; EOSINOPHILS; and NEUTROPHILS) as well as non-granular leukocytes (LYMPHOCYTES and MONOCYTES).
An angiotensin-converting enzyme inhibitor. It is used in patients with hypertension and heart failure.
Pathological processes of CORONARY ARTERIES that may derive from a congenital abnormality, atherosclerotic, or non-atherosclerotic cause.
Blood clot formation in any part of the CAROTID ARTERIES. This may produce CAROTID STENOSIS or occlusion of the vessel, leading to TRANSIENT ISCHEMIC ATTACK; CEREBRAL INFARCTION; or AMAUROSIS FUGAX.
An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.
A 12-KDa tacrolimus binding protein that is found associated with and may modulate the function of calcium release channels. It is a peptidyl-prolyl cis/trans isomerase which is inhibited by both tacrolimus (commonly called FK506) and SIROLIMUS.
An orphan nuclear receptor that is closely related to members of the thyroid-steroid receptor gene family. It was originally identified in NERVE CELLS and may play a role in mediation of NERVE GROWTH FACTOR-induced CELL DIFFERENTIATION. However, several other functions have been attributed to this protein including the positive and negative regulation of APOPTOSIS.
Nutrient blood vessels which supply the walls of large arteries or veins.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
A member of the family of TISSUE INHIBITOR OF METALLOPROTEINASES. It is a 21-kDa nonglycosylated protein found in tissue fluid and is secreted as a complex with progelatinase A by human fibroblast and uncomplexed from alveolar macrophages. An overexpression of TIMP-2 has been shown to inhibit invasive and metastatic activity of tumor cells and decrease tumor growth in vivo.
The physiological renewal, repair, or replacement of tissue.
Electropositive chemical elements characterized by ductility, malleability, luster, and conductance of heat and electricity. They can replace the hydrogen of an acid and form bases with hydroxyl radicals. (Grant & Hackh's Chemical Dictionary, 5th ed)
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
Agents that are used to treat allergic reactions. Most of these drugs act by preventing the release of inflammatory mediators or inhibiting the actions of released mediators on their target cells. (From AMA Drug Evaluations Annual, 1994, p475)
A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.
A secreted endopeptidase homologous with INTERSTITIAL COLLAGENASE, but which possesses an additional fibronectin-like domain.
A subcategory of structurally-related phospholipases A2 that do not require calcium for activity.
Implants constructed of materials designed to be absorbed by the body without producing an immune response. They are usually composed of plastics and are frequently used in orthopedics and orthodontics.
An NADPH-dependent enzyme that catalyzes the conversion of L-ARGININE and OXYGEN to produce CITRULLINE and NITRIC OXIDE.
Agents that antagonize ANGIOTENSIN RECEPTORS. Many drugs in this class specifically target the ANGIOTENSIN TYPE 1 RECEPTOR.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
A member of the family of TISSUE INHIBITOR OF METALLOPROTEINASES. It is a N-glycosylated protein, molecular weight 28 kD, produced by a vast range of cell types and found in a variety of tissues and body fluids. It has been shown to suppress metastasis and inhibit tumor invasion in vitro.
A technique that localizes specific nucleic acid sequences within intact chromosomes, eukaryotic cells, or bacterial cells through the use of specific nucleic acid-labeled probes.
A process involving chance used in therapeutic trials or other research endeavor for allocating experimental subjects, human or animal, between treatment and control groups, or among treatment groups. It may also apply to experiments on inanimate objects.
Surgical excision, performed under general anesthesia, of the atheromatous tunica intima of an artery. When reconstruction of an artery is performed as an endovascular procedure through a catheter, it is called ATHERECTOMY.
Microscopy in which the object is examined directly by an electron beam scanning the specimen point-by-point. The image is constructed by detecting the products of specimen interactions that are projected above the plane of the sample, such as backscattered electrons. Although SCANNING TRANSMISSION ELECTRON MICROSCOPY also scans the specimen point by point with the electron beam, the image is constructed by detecting the electrons, or their interaction products that are transmitted through the sample plane, so that is a form of TRANSMISSION ELECTRON MICROSCOPY.
A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of SKIN; CONNECTIVE TISSUE; and the organic substance of bones (BONE AND BONES) and teeth (TOOTH).
The development of new BLOOD VESSELS during the restoration of BLOOD CIRCULATION during the healing process.
A proteolytic enzyme that converts PLASMINOGEN to FIBRINOLYSIN where the preferential cleavage is between ARGININE and VALINE. It was isolated originally from human URINE, but is found in most tissues of most VERTEBRATES.
Specific receptors on cell membranes that react with PLATELET-DERIVED GROWTH FACTOR, its analogs, or antagonists. The alpha PDGF receptor (RECEPTOR, PLATELET-DERIVED GROWTH FACTOR ALPHA) and the beta PDGF receptor (RECEPTOR, PLATELET-DERIVED GROWTH FACTOR BETA) are the two principle types of PDGF receptors. Activation of the protein-tyrosine kinase activity of the receptors occurs by ligand-induced dimerization or heterodimerization of PDGF receptor types.
The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.
Reconstruction or repair of a blood vessel, which includes the widening of a pathological narrowing of an artery or vein by the removal of atheromatous plaque material and/or the endothelial lining as well, or by dilatation (BALLOON ANGIOPLASTY) to compress an ATHEROMA. Except for ENDARTERECTOMY, usually these procedures are performed via catheterization as minimally invasive ENDOVASCULAR PROCEDURES.
A member of the serpin family of proteins. It inhibits both the tissue-type and urokinase-type plasminogen activators.
A protein derived from FIBRINOGEN in the presence of THROMBIN, which forms part of the blood clot.
Synthetic or natural substances which are given to prevent a disease or disorder or are used in the process of treating a disease or injury due to a poisonous agent.
A minichromosome maintenance protein that is a key component of the six member MCM protein complex. It is also found in tightly-bound trimeric complex with MINICHROMOSOME MAINTENANCE COMPLEX COMPONENT 4 and MINICHROMOSOME MAINTENANCE COMPLEX COMPONENT 7.
A class of enzymes that catalyzes the degradation of gelatin by acting on the peptide bonds. EC 3.4.24.-.
A generic term used to describe a group of polypeptides with related chemical structures and pharmacological properties that are widely distributed in nature. These peptides are AUTACOIDS that act locally to produce pain, vasodilatation, increased vascular permeability, and the synthesis of prostaglandins. Thus, they comprise a subset of the large number of mediators that contribute to the inflammatory response. (From Goodman and Gilman's The Pharmacologic Basis of Therapeutics, 8th ed, p588)
The degree to which BLOOD VESSELS are not blocked or obstructed.
A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.
ENDOPEPTIDASES which use a metal such as ZINC in the catalytic mechanism.
A genus of the subfamily CERCOPITHECINAE, family CERCOPITHECIDAE, consisting of five named species: PAPIO URSINUS (chacma baboon), PAPIO CYNOCEPHALUS (yellow baboon), PAPIO PAPIO (western baboon), PAPIO ANUBIS (or olive baboon), and PAPIO HAMADRYAS (hamadryas baboon). Members of the Papio genus inhabit open woodland, savannahs, grassland, and rocky hill country. Some authors consider MANDRILLUS a subgenus of Papio.
A chemokine that is a chemoattractant for MONOCYTES and may also cause cellular activation of specific functions related to host defense. It is produced by LEUKOCYTES of both monocyte and lymphocyte lineage and by FIBROBLASTS during tissue injury. It has specificity for CCR2 RECEPTORS.
A high-molecular-weight plasma protein, produced by endothelial cells and megakaryocytes, that is part of the factor VIII/von Willebrand factor complex. The von Willebrand factor has receptors for collagen, platelets, and ristocetin activity as well as the immunologically distinct antigenic determinants. It functions in adhesion of platelets to collagen and hemostatic plug formation. The prolonged bleeding time in VON WILLEBRAND DISEASES is due to the deficiency of this factor.
An imbalance between myocardial functional requirements and the capacity of the CORONARY VESSELS to supply sufficient blood flow. It is a form of MYOCARDIAL ISCHEMIA (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels.
A technique for maintaining or growing TISSUE in vitro, usually by DIFFUSION, perifusion, or PERFUSION. The tissue is cultured directly after removal from the host without being dispersed for cell culture.
Radiography of the vascular system of the heart muscle after injection of a contrast medium.
Small double-stranded, non-protein coding RNAs (21-31 nucleotides) involved in GENE SILENCING functions, especially RNA INTERFERENCE (RNAi). Endogenously, siRNAs are generated from dsRNAs (RNA, DOUBLE-STRANDED) by the same ribonuclease, Dicer, that generates miRNAs (MICRORNAS). The perfect match of the siRNAs' antisense strand to their target RNAs mediates RNAi by siRNA-guided RNA cleavage. siRNAs fall into different classes including trans-acting siRNA (tasiRNA), repeat-associated RNA (rasiRNA), small-scan RNA (scnRNA), and Piwi protein-interacting RNA (piRNA) and have different specific gene silencing functions.
Cell surface proteins that bind ANGIOTENSINS and trigger intracellular changes influencing the behavior of cells.
Surgical insertion of BLOOD VESSEL PROSTHESES to repair injured or diseased blood vessels.
The number of CELLS of a specific kind, usually measured per unit volume or area of sample.
Drugs that are chemically similar to naturally occurring metabolites, but differ enough to interfere with normal metabolic pathways. (From AMA Drug Evaluations Annual, 1994, p2033)
A class of oxidized LDL receptors that contain LECTIN-like extracellular domains.
Coagulation of blood in any of the CORONARY VESSELS. The presence of a blood clot (THROMBUS) often leads to MYOCARDIAL INFARCTION.
Short fragments of DNA or RNA that are used to alter the function of target RNAs or DNAs to which they hybridize.
Adherence of cells to surfaces or to other cells.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
A subtype of non-receptor protein tyrosine phosphatases that includes two distinctive targeting motifs; an N-terminal motif specific for the INSULIN RECEPTOR, and a C-terminal motif specific for the SH3 domain containing proteins. This subtype includes a hydrophobic domain which localizes it to the ENDOPLASMIC RETICULUM.
Glycoproteins which contain sialic acid as one of their carbohydrates. They are often found on or in the cell or tissue membranes and participate in a variety of biological activities.
The vein accompanying the femoral artery in the same sheath; it is a continuation of the popliteal vein and becomes the external iliac vein.
Hexameric extracellular matrix glycoprotein transiently expressed in many developing organs and often re-expressed in tumors. It is present in the central and peripheral nervous systems as well as in smooth muscle and tendons. (From Kreis & Vale, Guidebook to the Extracellular Matrix and Adhesion Proteins, 1993, p93)
A CXC chemokine that is chemotactic for T-LYMPHOCYTES and MONOCYTES. It has specificity for CXCR4 RECEPTORS. Two isoforms of CXCL12 are produced by alternative mRNA splicing.
Organs, tissues, or cells taken from the body for grafting into another area of the same body or into another individual.
A family of structurally-related proteins that were originally identified by their ability to complex with cyclin proteins (CYCLINS). They share a common domain that binds specifically to F-BOX MOTIFS. They take part in SKP CULLIN F-BOX PROTEIN LIGASES, where they can bind to a variety of F-BOX PROTEINS.
Percutaneous transluminal procedure for removing atheromatous plaque from the coronary arteries. Both directional (for removing focal atheromas) and rotational (for removing concentric atheromatous plaque) atherectomy devices have been used.
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
The relationship between the dose of an administered drug and the response of the organism to the drug.
Surgical shunt allowing direct passage of blood from an artery to a vein. (From Dorland, 28th ed)
The venous trunk which receives blood from the lower extremities and from the pelvic and abdominal organs.
A cyclin-dependent kinase inhibitor that coordinates the activation of CYCLIN and CYCLIN-DEPENDENT KINASES during the CELL CYCLE. It interacts with active CYCLIN D complexed to CYCLIN-DEPENDENT KINASE 4 in proliferating cells, while in arrested cells it binds and inhibits CYCLIN E complexed to CYCLIN-DEPENDENT KINASE 2.
A gene silencing phenomenon whereby specific dsRNAs (RNA, DOUBLE-STRANDED) trigger the degradation of homologous mRNA (RNA, MESSENGER). The specific dsRNAs are processed into SMALL INTERFERING RNA (siRNA) which serves as a guide for cleavage of the homologous mRNA in the RNA-INDUCED SILENCING COMPLEX. DNA METHYLATION may also be triggered during this process.
The surgical removal of one or both ovaries.
Relatively undifferentiated cells that retain the ability to divide and proliferate throughout postnatal life to provide progenitor cells that can differentiate into specialized cells.
A pathologic process consisting of the proliferation of blood vessels in abnormal tissues or in abnormal positions.
Pathological processes involving any part of the AORTA.
Compounds containing 1,3-diazole, a five membered aromatic ring containing two nitrogen atoms separated by one of the carbons. Chemically reduced ones include IMIDAZOLINES and IMIDAZOLIDINES. Distinguish from 1,2-diazole (PYRAZOLES).
A cyclodecane isolated from the bark of the Pacific yew tree, TAXUS BREVIFOLIA. It stabilizes MICROTUBULES in their polymerized form leading to cell death.
Derivatives of propionic acid. Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain the carboxyethane structure.

Recombinant human interleukin-10 inhibits proliferation of vascular smooth muscle cells stimulated by advanced glycation end products and neointima hyperplasia after carotid injury in the rat. (1/339)

The purposes of this study was to determine the effects of recombinant human interleukin-10 (rhIL-10) on proliferation of vascular smooth muscle cells (VSMCs) stimulated by advanced glycation end products (AGE) and neointima hyperplasia after rat carotid arterial injury. Rat aortic VSMCs were cultured and treated with rhIL-10 or AGE respectively, and then co-treated with rhIL-10 and AGE. Proliferation of VSMCs was quantified by colormetric assay. Cell cycle analysis was performed by flow cytomertry. Sprague-Dawley rats were treated with recombinant human IL-10 (rhIL-10) for 3 d after carotid arteries injury. The ratio of neointima to media area at the site of arterial injury was measured 28 d after balloon injury. The p44/42 MAPK activity was evaluated by the immunoblotting technique using anti-p44/42 phospho-MAPK antibody. Compared to control, AGE stimulated VSMCs proliferation. rhIL-10 alone had no effect on VSMCs growth. With AGE stimulation, rhIL-10, at dose as low as 10 ng/ml, inhibited VSMCs growth (P<0.05). The cell number in G(0)/G(1) phase of AGE and rhIL-10 co-treatment group was higher than that of AGE treatment alone (P<0.01) by flow cytometry analysis. Compared with the control group of neointima hyperplasia in rats, the ratio of neointima to media area of recombinant human IL-10 group was reduced by 45% (P<0.01). The p44/42 MAPK activity was significantly enhanced by AGE. The AGE effects were opposed by rhIL-10. The anti-inflammatory cytokine rhIL-10 inhibits AGE-induced VSMCs proliferation. Recombinant human IL-10 also inhibited neointima hyperplasia after carotid artery injury in rats. The results suggest the possibility that recombinant human IL-10, as a potential therapeutic approach, prevents neointimal hyperplasia.  (+info)

Novel neointimal formation over sirolimus-eluting stents identified by coronary angioscopy and optical coherence tomography. (2/339)

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A case of a newly developed yellow neointima at stent implanted site 1 year after sirolimus-eluting stent placement: angioscopic findings. (3/339)

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Effect of alpha lipoic acid in a porcine in-stent restenosis model. (4/339)

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Blockade of TGF-beta by catheter-based local intravascular gene delivery does not alter the in-stent neointimal response, but enhances inflammation in pig coronary arteries. (5/339)

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A20 inhibits post-angioplasty restenosis by blocking macrophage trafficking and decreasing adventitial neovascularization. (6/339)

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Local arterial nanoparticle delivery of siRNA for NOX2 knockdown to prevent restenosis in an atherosclerotic rat model. (7/339)

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Mechanisms of vein graft adaptation to the arterial circulation: insights into the neointimal algorithm and management strategies. (8/339)

For patients with coronary artery disease or limb ischemia, placement of a vein graft as a conduit for a bypass is an important and generally durable strategy among the options for arterial reconstructive surgery. Vein grafts adapt to the arterial environment, and the limited formation of intimal hyperplasia in the vein graft wall is thought to be an important component of successful vein graft adaptation. However, it is also known that abnormal, or uncontrolled, adaptation may lead to abnormal vessel wall remodeling with excessive neointimal hyperplasia, and ultimately vein graft failure and clinical complications. Therefore, understanding the venous-specific pathophysiological and molecular mechanisms of vein graft adaptation are important for clinical vein graft management. Of particular importance, it is currently unknown whether there exist several specific distinct molecular differences in the venous mechanisms of adaptation that are distinct from arterial post-injury responses; in particular, the participation of the venous determinant Eph-B4 and the vascular protective molecule Nogo-B may be involved in mechanisms of vessel remodeling specific to the vein. This review describes (1) venous biology from embryonic development to the mature quiescent state, (2) sequential pathologies of vein graft neointima formation, and (3) novel candidates for strategies of vein graft management. Scientific inquiry into venous-specific adaptation mechanisms will ultimately provide improvements in vein graft clinical outcomes.  (+info)

TY - JOUR. T1 - Deletion of Krüppel-like factor 4 in endothelial and hematopoietic cells enhances neointimal formation following vascular injury.. AU - Yoshida, Tadashi. AU - Yamashita, Maho. AU - Horimai, Chihiro. AU - Hayashi, Matsuhiko. PY - 2014. Y1 - 2014. N2 - Krüppel-like factor 4 (Klf4) is involved in a variety of cellular functions by activating or repressing the transcription of multiple genes. Results of previous studies showed that tamoxifen-inducible global deletion of the Klf4 gene in mice accelerated neointimal formation following vascular injury, in part via enhanced proliferation of smooth muscle cells (SMCs). Because Klf4 is also expressed in non-SMCs including endothelial cells (ECs), we determined if Tie2 promoter-dependent deletion of Klf4 in ECs and hematopoietic cells affected injury-induced neointimal formation. Klf4 conditional knockout (cKO) mice were generated by breeding Tie2-Cre mice and Klf4 floxed mice, and their phenotype was analyzed after carotid ligation ...
Heterogeneous neointima were detected in 21.5% of DES-treated lesions in the study population. The occurrence of neointimal tissue in this group was significantly associated with both advanced age and initial clinical presentation of acute coronary syndrome. MACE occurred more frequently in patients in the heterogeneous group compared with those in the nonheterogeneous group during the average 31-month follow-up period (13.7% vs. 2.9% in the homogeneous group vs. 7.3% in the layered group, p = 0.001). In addition, we found that inclusion in the heterogeneous group and minimal lumen CSA on follow-up OCT examination were independent risk factors for future MACE. To the best of our knowledge, this is the first study to investigate the clinical significance of neointimal tissue patterns without features of neoatherosclerosis. Our data suggest that the heterogeneous neointimal tissue pattern is correlated with poor long-term clinical outcomes.. OCT is a valuable intravascular imaging modality for ...
It has been shown that angiotensinII receptor blocker (ARB) has an inhibitory effect on neointima formation. Bone marrow-derived mononuclear cells (BM-MNCs) which express angiotensinII (AngII) type 1 receptor (AT1R) have been shown to give rise to smooth muscle(SM) like cells at injured vascular walls. However, the role of AngII in the process of BM-MNC incorporation to neointimal formation is little known. Human peripheral blood mononuclear cells (PB-MNCs) were cultured in the presence of PDGF-BB and basic FGF. Immunohistochemistry and RT-PCR revealed that PB-MNCs gave rise to SM-like cells. Immunohistochemistry revealed that αSMA, SM1 and SMemb become positive in PB-MNC derived SM-like cells. RT-PCR confirmed the expression of αSMA, SMemb and AT1R mRNA in PB-MNC derived SM- like cells. The number of SM-like progenitor cells were increased by AngII, and this was blocked by an ARB CV-11974(αSMA+cell/ HPF: 32.6±3.3, 23.4±2.3 vs. 19.0±2.0, P,0.001). CV-11974 alone further decreased the ...
The goal of this project is to define the role of peroxisome proliferator-activated receptor (PPAR)3 activation in neointima formation. Neointima formation occu...
Based on our previous results implicating CaMKIIδ2 as regulator of cell migration and proliferation in cultured rat aortic VSM cells,16,18 we investigated the function of CaMKIIδ2 in the vascular response to injury. Consistent with results using an in vitro system,18 we observed a rapid and marked modulation in vascular wall CaMKII isoform expression after balloon injury in vivo, coinciding with acquisition of a migratory/proliferative phenotype in both carotid artery medial VSM and adventitial fibroblasts. Inhibiting acute upregulation of the CaMKIIδ2 isoform attenuated migration and proliferation, and functionally suppressed neointima formation and adventitial thickening. We conclude from these studies that CaMKIIδ isoforms specifically couple Ca2+ signals to regulate cell migration and proliferation, and that increased expression of these isoforms in VSM or adventitial myofibroblasts is an important component of injury induced vascular wall remodeling.. Potential sources of neointimal VSM ...
OSU Libraries and Press Research Data Services provides guidance and support for all aspects of the research data lifecycle, from planning your data management strategy during the proposal phase through preserving your data at the conclusion of your project. Our services are free of charge, and we are happy to partner with you on proposals and projects. Our guide to Research Data Services offers support for managing data, creating and maintaining metadata and documentation, and services for data sharing and preservation.. ...
OBJECTIVES: We used optical coherence tomography, which has a resolution of |20 microm, to analyze thin layers of neointima in rapamycin-eluting coronary stents. BACKGROUND: Lack of neointimal coverage has been implicated in the pathogenesis of drug-eluting coronary stent thrombosis. Angiography and intracoronary ultrasound lack the resolution to examine this. METHODS: We conducted a randomized trial in patients receiving polymer-coated rapamycin-eluting stents (Cypher, Cordis, Johnson & Johnson, Miami, Florida) and nonpolymer rapamycin-eluting stents (Yukon, Translumina, Hechingen, Germany) to examine neointimal thickness, stent strut coverage, and protrusion at 90 days. Twenty-four patients (n = 12 for each group) underwent stent deployment and invasive follow-up at 90 days with optical coherence tomography. The primary end point was binary stent strut coverage. Coprimary end points were neointimal thickness and stent strut luminal protrusion. RESULTS: No patient had angiographic restenosis. For
TY - JOUR. T1 - The APOSTEL recommendations for reporting quantitative optical coherence tomography studies. AU - Cruz-Herranz, Andrés. AU - Balk, Lisanne J.. AU - Oberwahrenbrock, Timm. AU - Saidha, Shiv. AU - Martinez-Lapiscina, Elena H.. AU - Lagreze, Wolf A.. AU - Schuman, Joel S.. AU - Villoslada, Pablo. AU - Calabresi, Peter. AU - Balcer, Laura. AU - Petzold, Axel. AU - Green, Ari J.. AU - Paul, Friedemann. AU - Brandt, Alexander U.. AU - Albrecht, Philipp. PY - 2016/6/14. Y1 - 2016/6/14. N2 - Objective: To develop consensus recommendations for reporting of quantitative optical coherence tomography (OCT) study results. Methods: A panel of experienced OCT researchers (including 11 neurologists, 2 ophthalmologists, and 2 neuroscientists) discussed requirements for performing and reporting quantitative analyses of retinal morphology and developed a list of initial recommendations based on experience and previous studies. The list of recommendations was subsequently revised during several ...
OCT data analysis was performed offline using proprietary software (LightLab Imaging Inc.). Analysis of angiographic images, quantitative coronary angiography (Medis, Leiden, the Netherlands), and OCT was performed by experienced investigators (P.B. and P.M.). Regarding blinding, the very different presentation of the 2 stent types (including, in particular, the hub of the devices and the angiographic appearances of the markers) made it impractical to blind the operators; however, for the angiographic and OCT analysis, investigators were blinded to the randomization arm. The analyst was blinded to all clinical and procedural variables and thus, did not have any knowledge of stent sizes or stent type. When a strut was felt to be malapposed, the distance from the strut to lumen surface was recorded. Only after completion of the analysis was the stent type used to then confirm the presence or absence of malapposition by incorporating the actual strut thickness for the 2 stents used. This is ...
The question of whether DES are safe, has become an area of considerable interest and controversy with the publication of a relatively small randomized trial (BASKET-LATE), an observational study and a meta-analysis reporting increased rates of ST, MI, and death with DES compared to BMS. The motivating factor was the presentation of a meta-analysis at the European Society of Cardiology meeting in Barcelona in September 2006, which suggested an increase in the risk of death and MI following implantation of sirolimus-eluting stents.. The major issue in these meta-analyses is that they were limited either by small sample sizes, duration of follow-ups, lack of access to source data, or by using landmark analyses that excluded events in first 6 months.. Moreover, the largest meta-analysis of DES vs. BMS and SES vs. PES published recently in The Lancet by Settler et al performed a network analyses with a mixed-treatment comparison of 38 randomized trials (18023 patients) with a follow-up of up to 4 ...
Our study demonstrated that vulnerable plaque characteristics, including thinner fibrous cap, greater lipid arc, longer lipid core length, and TCFA, were seen more frequently in UAP culprit lesions with NV when compared with those without NV, but not in the non-culprit lesions of UAP and in the lesions of SAP.. In this study, we observed NV in 35% of the culprit lesions in UAP patients. This finding is consistent with the previous report by Kitabata et al,9 where NV was found in 38% of the culprit lesions in UAP patients. NV was observed in 34% of non-culprit lesions and in 28% of the lesions in SAP patients. The difference was not significant between the three groups. Our findings, which associate NV with the presence of TCFA, thinner fibrous cap, and larger plaque burden, are also in good agreement with the previous report.9 The results obtained from the study by Fujii K et al13 have shown that ruptured plaques in culprit lesions of patients with acute coronary syndromes have greater plaque ...
The aim of the APOSTEL recommendations is to provide a consistent basis for assisting authors in composing conclusive reports of studies utilizing quantitative retinal OCT, allowing relevant comparisons across and between studies, and helping readers, reviewers, and editors to evaluate these findings. Furthermore, by emphasizing details that are of importance in such reports, we hope to generally improve the quality of future investigations in this area. Defining the relevant parameters for reporting may prompt researchers to thoroughly consider these criteria during the initial stages of study design. Such an approach could help facilitate OCT research in centers intending to incorporate OCT for clinical trials or other research purposes. Adherence to the recommendations can help avoid common pitfalls in the design and reporting of OCT studies. These recommendations are not intended to impose a rigid format on reports of OCT-based research, but rather to provide suggestions and guidance on ...
Fibronectin-splice variant containing extra domain A (Fn-EDA) is associated with smooth muscle cells (SMCs) following vascular injury. The role of SMC-derived Fn-EDA in SMC phenotypic switching or its implication in neointimal hyperplasia remains unclear. Herein, using human coronary artery sections with a bare metal stent, we demonstrate the expression of Fn-EDA in the vicinity of SMC-rich neointima and peri-strut areas. In mice, Fn-EDA colocalizes with SMCs in the neointima of injured carotid arteries and promotes neointima formation in the comorbid condition of hyperlipidemia by potentiating SMC proliferation and migration. No sex-based differences were observed. Mechanistic studies suggested that Fn-EDA mediates integrin- and TLR4-dependent proliferation and migration through activation of FAK/Src and Akt1/mTOR signaling, respectively. Specific deletion of Fn-EDA in SMCs, but not in endothelial cells, reduced intimal hyperplasia and suppressed the SMC synthetic phenotype concomitant with ...
CVE-2018-11776 operates at a far deeper level within the code than all prior Struts vulnerabilities. This requires a greater understanding of the ...
Background: Reendothelialization following vascular injury after balloon angioplasty or stent implantation is clinically extremely relevant to promote vascular healing and prevent fatal events such as stent thrombosis and restenosis. We already identified the importance of Toll-like receptor (TLR) 2/6 for endothelial regeneration. We now investigated the therapeutic potential of the TLR2/6 agonist MALP-2 on reendothelialization in a murine model of vascular injury. Methods and Results: The left common carotid artery of C57BL/6N mice was experimentally injured and reendothelialization was quantified by Evans Blue staining after 3 days in en face prepared vessels. A single intravenous injection of MALP-2 (1 or 10 µg) following vascular injury dose-dependently accelerated reendothelialization up to 3.5-fold (n=12-18, P,0.001) which was abolished by administration of neutralizing antibodies against TLR2 and TLR6. Proliferation of endothelial cells at the wound margins determined by ...
Neurofibromin 2 (NF2), a potent tumor suppressor, is reported to inhibit proliferation in several cell types. The role of NF2 in neointima hyperplasia after vascular injury is unknown. We explored the role of NF2 in proliferation, migration of vascular smooth muscle cell (VSMC) and neointima hyperplasia after vascular injury. NF2 phosphorylation was elevated in VSMC subjected to platelet-derived growth factor (PDGF)-BB and in artery subjected to vascular injury. Mice deficient for Nf2 in VSMC showed enhanced neointima hyperplasia after injury, increased proliferation and migration of VSMC after PDGF-BB treatment. Mechanistically, we observed increased nuclear p-NF2, declined p-Yes-Associated Protein (YAP), nuclear translocation of YAP after PDGF-BB treatment or injury. NF2 knockdown or YAP overexpression showed similar phenotype in VSMC proliferation, migration and neointima hyperplasia. YAP inhibition abolished the above effects mediated by NF2 knockdown. Finally, NF2 knockdown further promoted
Results All endovascular procedures and OCT pullback runs were feasible. Stent apposition was satisfactory on the immediate post-stent OCT reconstructions. At 12-week controls, all stents and jailed branches were patent. Mean neointimal thickness was 0.11±0.04 mm on the free segments of the stent. The mean ostia surface at 12 weeks was 319 750±345 533 μm2 with 3D-OCT reconstructions and 351 198±396 355 μm2 with SEM image-derived calculations. Good correlation was found for ostia surface values between the two techniques; the values did not differ significantly in this preliminary study. ...
DESIGN:. Imaging and vasomotion Substudy:. 50 consecutive patients enrolled in the COMPARE II trial at the University of Fribourg Medical Center will undergo follow-up re-angiography 14 months after index procedure with assessment of Optical coherence tomography (OCT) and vasomotion testing.. ENDPOINT SUBSTUDY (all at 14 months):. Primary endpoint imaging: percentage of uncovered stent struts per lesion and mean neointimal thickness assessed by OCT.. vasomotion: coronary vasomotion assessed with quantitative coronary angiography at rest and during supine bicycle exercise. ...
Our study addressed the question of whether or not expression of vWF influenced neointimal formation in arteries with altered shear stress. We found that the absence of vWF did not alter the size of the neointimal lesions, the number of layers of cells in the neointima, or the expression of PCNA in the neointima or media. The exact mechanism of neointimal formation in arteries with altered shear stress is unknown but is likely to be multifactorial. It has been known for some time that many forms of vascular manipulation will induce neointimal formation, and there appear to be important species-dependent responses (reviewed in References 30 through 3230 31 32 ). First, simple surgical isolation of an artery induces neointima in rabbits, and thus, either the operative procedure alone or the disturbed flow that likely occurs during healing contributes to neointimal hyperplasia.33 Second, vascular injury applied either externally to a rabbit artery or endoluminally in rats, rabbits, and pigs induces ...
Three-dimensional morphological response of lipid-rich coronary plaques to statin therapy: a serial optical coherence tomography study
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
Medical definition of neointima: a new or thickened layer of arterial intima formed especially on a prosthesis or in atherosclerosis by migration and proliferation of cells from the media.
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While not always apparent, as the vehicle's mileage climbs, its strut mounts often deteriorate. Therefore, when the struts are being replaced (especially on high mileage vehicles), it's also the perfect time to replace the strut mounts in order to help restore the vehicle's like-new...
While not always apparent, as the vehicle's mileage climbs, its strut mounts often deteriorate. Therefore, when the struts are being replaced (especially on high mileage vehicles), it's also the perfect time to replace the strut mounts in order to help restore the vehicle's like-new...
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Neointimal hyperplasia refers to proliferation and migration of vascular smooth muscle cells primarily in the tunica intima, resulting in the thickening of arterial walls and decreased arterial lumen space. Neointimal hyperplasia is the major cause of restenosis after percutaneous coronary interventions such as stenting or angioplasty. The term neointima is used because the cells in the hyperplastic regions of the vascular wall have histological characteristics of both intima and normal artery cells. Neointimal hyperplasia first develops with damage to the arterial wall, followed by platelet aggregation at site of injury, recruitment of inflammatory cells, proliferation and migration of vascular smooth muscle cells, and collagen deposition. Mechanical injury of arterials due to stretching of arterial walls with a balloon catheter results in the recruitment of cells such as monocytes, macrophages, and neutrophils to the site of injury. Macrophages in particular express many growth factors, ...
Fibronectin-splice variant containing extra domain A (Fn-EDA) is associated with smooth muscle cells (SMCs) following vascular injury. The role of SMC-derived Fn-EDA in SMC phenotypic switching or its implication in neointimal hyperplasia remains unclear. Herein, using human coronary artery sections with a bare metal stent, we demonstrate the expression of Fn-EDA in the vicinity of SMC-rich neointima and peri-strut areas. In mice, Fn-EDA colocalizes with SMCs in the neointima of injured carotid arteries and promotes neointima formation in the comorbid condition of hyperlipidemia by potentiating SMC proliferation and migration. No sex-based differences were observed. Mechanistic studies suggested that Fn-EDA mediates integrin- and TLR4-dependent proliferation and migration through activation of FAK/Src and Akt1/mTOR signaling, respectively. Specific deletion of Fn-EDA in SMCs, but not in endothelial cells, reduced intimal hyperplasia and suppressed the SMC synthetic phenotype concomitant with ...
Fibronectin-splice variant containing extra domain A (Fn-EDA) is associated with smooth muscle cells (SMCs) following vascular injury. The role of SMC-derived Fn-EDA in SMC phenotypic switching or its implication in neointimal hyperplasia remains unclear. Herein, using human coronary artery sections with a bare metal stent, we demonstrate the expression of Fn-EDA in the vicinity of SMC-rich neointima and peri-strut areas. In mice, Fn-EDA colocalizes with SMCs in the neointima of injured carotid arteries and promotes neointima formation in the comorbid condition of hyperlipidemia by potentiating SMC proliferation and migration. No sex-based differences were observed. Mechanistic studies suggested that Fn-EDA mediates integrin- and TLR4-dependent proliferation and migration through activation of FAK/Src and Akt1/mTOR signaling, respectively. Specific deletion of Fn-EDA in SMCs, but not in endothelial cells, reduced intimal hyperplasia and suppressed the SMC synthetic phenotype concomitant with ...
TY - JOUR. T1 - A proliferation analysis of arterial neointimal hyperplasia. T2 - Lessons for antiproliferative restenosis therapies. AU - Schwartz, Robert S.. AU - Chu, Aloysius. AU - Edwards, William D.. AU - Srivatsa, Sanjay S.. AU - Simari, Robert D.. AU - Isner, Jeffrey M.. AU - Holmes, David R.. PY - 1996/1. Y1 - 1996/1. N2 - Medial smooth muscle cell proliferation is frequently implicated as the major cause of coronary restenosis. Although antiproliferative agents have shown efficacy in animal studies, they are ineffective in human trials. To better understand these discrepancies, we performed a mathematical kinetic analysis of cellular proliferation in the neointimal hyperplasia of rats, pigs, and patients. A model was derived using a differential expression for proliferation, proportional to the number of cells present. Additional terms were included for inhibition of proliferation proportional to neointimal mass and time. The resulting equation was solved in closed form for the number ...
Lipoprotein (a) level is associated with plaque vulnerability in patients with coronary artery disease: An optical coherence tomography study
PhD Project - Exploring the similarities between neointimal formation after vascular injury and tumour growth at University of Bristol, listed on FindAPhD.com
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Bilirubin is a heme metabolite generated by the concerted action of the enzymes heme oxygenase and biliverdin reductase. Although long considered a toxic byproduct of heme catabolism, recent preclinical, and clinical studies indicate the bilirubin exerts beneficial effects in the circulation. In the present study, we determined whether local administration of bilirubin attenuates neointima formation following injury of rat carotid arteries. In addition, the ability of bilirubin to regulate the proliferation and migration of human arterial smooth muscle cells (SMCs) was investigated. Local perivascular administration of bilirubin immediately following balloon injury of rat carotid arteries significantly attenuated neointima formation. Bilirubin-mediated inhibition of neointimal thickening was associated with a significant decrease in ERK activity and cyclin D1 and A protein expression, and an increase in p21 and p53 protein expression in injured blood vessels. Treatment of human aortic SMCs with ...
TY - JOUR. T1 - Protective Aptitude of Annexin A1 in Arterial Neointima Formation in Atherosclerosis-Prone Mice-Brief Report. AU - de Jong, Renske J.. AU - Paulin, Nicole. AU - Lemnitzer, Patricia. AU - Viola, Joana R.. AU - Winter, Carla. AU - Ferraro, Bartolo. AU - Grommes, Jochen. AU - Weber, Christian. AU - Reutelingsperger, Chris. AU - Drechsler, Maik. AU - Soehnlein, Oliver. PY - 2017/2. Y1 - 2017/2. KW - annexin A1. KW - macrophage. KW - neointima formation. KW - resolution of inflammation. KW - INFLAMMATION. KW - RECRUITMENT. U2 - 10.1161/ATVBAHA.116.308744. DO - 10.1161/ATVBAHA.116.308744. M3 - Article. VL - 37. SP - 312. EP - 315. JO - Arteriosclerosis Thrombosis and Vascular Biology. JF - Arteriosclerosis Thrombosis and Vascular Biology. SN - 1079-5642. IS - 2. ER - ...
Fingerprint Dive into the research topics of Comparisons of the effects of stent eccentricity on the neointimal hyperplasia between Sirolimus-eluting stent versus Paclitaxel-eluting stent. Together they form a unique fingerprint. ...
B,Accumulating evidence shows that inhibition of the vascular renin-angiotensin system results in suppression of injury-elicited neointima formation. We attempted to determine whether or not combined treatment with an angiotensin II type 1 receptor blocker (ARB) and angiotensin converting enzyme inhibitor (ACEI) has an additive inhibitory effect on balloon-injury-elicited neointima formation in the carotid artery. Male Sprague-Dawley rats were treated with an ARB (valsartan: 3 mg/kg/day) and/or an ACEI (benazepril: 0.3 mg/kg/day) from 1 week before until 2 weeks after balloon injury. Experiments were also conducted with one-third of the dose combination used in the original experiments. Both ARB and ACEI inhibited neointima formation without any blood pressure changes. The full-dose combination lowered blood pressure and suppressed neointima formation significantly compared with the levels in the groups treated with either ACEI or ARB alone. The low-dose combination without blood pressure ...
Sigma-Aldrich offers abstracts and full-text articles by [Nick D Tsihlis, Muneera R Kapadia, Ashley K Vavra, Walker D Flannery, Christopher S Oustwani, Qun Jiang, Melina R Kibbe].
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Thank you for taking the time to nominate a fellow for TCTMDs Featured Fellow section on the Fellows Forum. Nominees should be current general or interventional cardiology fellows who you have supervised or mentored and think should be recognized for a combination of their scholarship, skills, talent, and commitment to top-notch patient care. If your nominee is selected, you will be notified of our selection and alerted when the story appears on TCTMD. Please email [email protected] with any questions ...
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When I picked up the box off the front porch, I Thought, maybe this isnt the strong strut, or if it is, maybe they forgot to put in in the box! The dang thing is super super light. I didnt bother to weigh it, but let me tell you, its impressively light. ...
Purpose: To determine the choroidal thickness (CT) profile in keratoconus (KC) patients using swept-source optical coherence tomography (SS-OCT). Methods: This was a prospective, cross-sectional study. One hundred two eyes of 52 KC patients were studied using Pentacam and SS-OCT. The macular CT profile was created by manually measuring the distance between the retinal pigment epithelium and the choroid-sclera junction on horizontal b-scans at nine different macular locations. The results were compared to 93 eyes of 93 healthy controls. Results: Mean age of the KC group was 34.9 ± 13.5 years and mean axial length (AL) was 24.1 ± 1.3 mm. Mean topographic KC classification (TKC) was 2.0; 39 eyes were classified as early KC (TKC ,1-2), 34 eyes as moderate (TKC 2, 2-3), and 29 as advanced (TKC 3+). Mean subfoveal CT was 383.2 μm in KC patients and 280.5 μm in control group (P , 0.001). CT in KC patients was statistically thicker in all measure locations (P , 0.001). CT in KC eyes decreased with ...
title: Optical coherence tomographic observation of morphological features of neointimal tissue after drug-eluting stent implantation., doi: 10.3349/ymj.2014.55.4.944, category: Article
ObjectiveIn balloon-injured rat carotid arteries, angiotensin-converting enzyme inhibitors (ACEI) decrease neointima formation, and a kinin receptor antagonist partially reverses this inhibitory effect. We studied which of the events leading to neointima formation are involved in the effects of ACEI
Principal Investigator:SAKUMA Makoto, Project Period (FY):1989 - 1990, Research Category:Grant-in-Aid for General Scientific Research (C), Research Field:General surgery
Technavio analysts forecast the global drug-eluting balloons market to grow to USD 664.35 million by 2021, at a CAGR of more than 27%.
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Using MFAP4-deficient mouse models, studies have shown roles for MFAP4 in neointima formation and asthma. Moreover, it has ... Jan 2016). "MFAP4 Promotes Vascular Smooth Muscle Migration, Proliferation and Accelerates Neointima Formation". ...
... the so-called neointima. Development of a neointima is variable but can at times be so severe as to re-occlude the vessel lumen ... Consequently, current research focuses on the reduction of neointima after stent placement. Substantial improvements have been ...
... mouse show reduced neointima formation. The association of ADAMTS7 with atherosclerosis suggests that inhibition of ADAMTS7 ... "ADAMTS-7 mediates vascular smooth muscle cell migration and neointima formation in balloon-injured rat arteries". Circulation ...
... migration and neointima formation after arterial injury". J. Cardiovasc. Pharmacol. 42 (4): 469-76. doi:10.1097/00005344- ...
"Previously differentiated medial vascular smooth muscle cells contribute to neointima formation following vascular injury". ...
... expression in arterial wall after balloon angioplasty correlates with late stages of neointima formation and ... the exact role of T-cadherin in neointima formation and atherosclerosis development is poorly understood. LDL is not the only ...
August 2010). "Cellular mechanisms by which proinsulin C-peptide prevents insulin-induced neointima formation in human ...
"LincRNA-p21 regulates neointima formation, vascular smooth muscle cell proliferation, apoptosis, and atherosclerosis by ...
"Adenoviral expression of a urokinase receptor-targeted protease inhibitor inhibits neointima formation in murine and human ...
... upregulated during neointima formation in a rat carotid endarterectomy model". Biochimica et Biophysica Acta (BBA) - Gene ...
Khachigian, L.M. et al (2002) c-Jun regulates vascular smooth muscle cell growth and neointima formation after arterial injury ...
... a paclitaxel coating limits the growth of neointima (scar tissue) within stents. Paclitaxel drug-eluting stents for coronary ...
"Desalted Salicornia europaea extract attenuated vascular neointima formation by inhibiting the MAPK pathway-mediated migration ...
... porous polyester stent reduces vein graft neointima formation, cholesterol concentration, and vascular cell adhesion molecule 1 ...
"Adenovirus-mediated gene transfer of human platelet-activating factor-acetylhydrolase prevents injury-induced neointima ...
The term neointima is used because the cells in the hyperplastic regions of the vascular wall have histological characteristics ...
... is overexpressed in vascular smooth muscle cells of atherosclerotic lesions and in the neointima of restenosis after ...
... which was shown to suppress proliferation of vascular smooth muscle cells and to reduce neointima formation in mouse restenosis ...
Functional neointima characterization of vascular prostheses in human. Ann Thorac Surg. 2004; 77: 864-8 Walles T, Giere B, ...
... can form as a result of vascular surgery such as angioplasty or stent placement. It is actually due to proliferation ... Neointima typically refers to scar tissue that forms within tubular anatomical structures such as blood vessels, as the intima ...
Neointima can form as a result of vascular surgery such as angioplasty or stent placement. It is actually due to proliferation ... Neointima typically refers to scar tissue that forms within tubular anatomical structures such as blood vessels, as the intima ...
Medical definition of neointima: a new or thickened layer of arterial intima formed especially on a prosthesis or in ... Learn More about neointima. Share neointima Post the Definition of neointima to Facebook Share the Definition of neointima on ... Comments on neointima What made you want to look up neointima? Please tell us where you read or heard it (including the quote, ... Dictionary Entries near neointima. neo-Freudian neogenetic neohesperidin dihydrochalcone neointima neologism neomorph neomycin ...
Figure 2 : SRSF1 deficiency in VSMCs inhibits neointima formation.. From: SRSF1 promotes vascular smooth muscle cell ... neointima; M, media); n=9 per group. (e,f) Representative photomicrographs of immunohistochemical staining (scale bar, 25 μm) ( ... neointima/media ratio, media area and circumference of external elastic lamina (EEL) of carotid arteries from Srsf1−/− and WT ...
neointima definition: Noun (plural neointimas or neointimae) 1. (anatomy) A new layer of arterial intima, especially that ... neointima. Noun (plural neointimas or neointimae). *(anatomy) A new layer of arterial intima, especially that formed on a ... How would you define neointima? Add your definition here.. Please enable JavaScript to view the comments powered by Disqus.. ...
Abstract 14668: Epac1 Deficiency Inhibit Neointima Formation After Vascular Injuryin vivo. Yuko Kato, Utako Yokoyama, Satoshi ... Conclusion:These results suggest that Epac1 deficiency inhibit neointima formation after vascular injury in vivo. ... Abstract 14668: Epac1 Deficiency Inhibit Neointima Formation After Vascular Injuryin vivo ... Abstract 14668: Epac1 Deficiency Inhibit Neointima Formation After Vascular Injuryin vivo ...
C1-esterase inhibitor protects against neointima formation after arterial injury in atherosclerosis-prone mice. ... Search: C1[Title] AND esterase[Title] AND inhibitor[Title] AND protects[Title] AND against[Title] AND neointima[Title] AND ... C1[Title] AND esterase[Title] AND inhibitor[Title] AND protects[Title] AND against[Title] AND neointima[Title] AND formation[ ... Search: C1 esterase inhibitor protects against neointima formation aft.... *. Number of items displayed:. 5. 10. 15. 20. 50. ...
The apparent number of these receptors was fourfold higher in the neointima compared to that in the normal aortic wall. The ... Angiotensin-converting enzyme binding in the neointima was not different from that in the media of the uninjured aorta. Our ... Balloon angioplasty enhances the expression of angiotensin II AT1 receptors in neointima of rat aorta.. ... Balloon angioplasty enhances the expression of angiotensin II AT1 receptors in neointima of rat aorta.. ...
March 2018): Deletion of MFGE8 Inhibits Neointima Formation upon Arterial Damage. In: Thrombosis and Haemostasis, Vol. 118, No ...
Abstract 20944: Perivascular Progenitor Cells Contribute To Neointima Formation After Wire-induced Injury. Jan-Marcus Daniel, ... In conclusion, we provide evidence that BMPCs within the neointima rarely co-express markers for vascular cells and do not ... Most of the accumulating EGFP+-cells were identified as inflammatory cells (CD45, CD68), and their number in the neointima ... Abstract 20944: Perivascular Progenitor Cells Contribute To Neointima Formation After Wire-induced Injury ...
Whether AMPK alpha alters vascular neointima formation induced by vascular injury is unknown.Objective: The aim of this study ... Finally, neointima formation after mechanical arterial injury was increased in AMPK alpha 2(-/-) but not AMPK alpha 1(-/-) mice ... Objective: The aim of this study was to determine the roles of AMPK alpha in the development of vascular neointima hyperplasia ... Song, P., Wang, S., He, C., Wang, S., Liang, B., Viollet, B., & Zou, M-H. (2011). AMPK alpha 2 deletion exacerbates neointima ...
Arginase Promotes Neointima Formation in Rat Injured Carotid Arteries. Kelly J. Peyton, Diana Ensenat, Mohammed A. Azam, Amit N ... Arginase Promotes Neointima Formation in Rat Injured Carotid Arteries. Kelly J. Peyton, Diana Ensenat, Mohammed A. Azam, Amit N ... Arginase Promotes Neointima Formation in Rat Injured Carotid Arteries. Kelly J. Peyton, Diana Ensenat, Mohammed A. Azam, Amit N ...
When one considers, however, the percentage of neointima actually removed, even with the largest rotablator burrs, the commonly ... New recipes for in-stent restenosis: cut, grate, roast, or sandwich the neointima? ... New recipes for in-stent restenosis: cut, grate, roast, or sandwich the neointima? ... removal of neointima is the best method of treating in-stent restenosis but, in order for it to be practical and effective, new ...
Animals treated with empty gel exhibited a significant and concentric neointima. In contrast, a markedly diminished neointima ... Arginase Promotes Neointima Formation in Rat Injured Carotid Arteries. Kelly J. Peyton, Diana Ensenat, Mohammed A. Azam, Amit N ... Arginase Promotes Neointima Formation in Rat Injured Carotid Arteries. Kelly J. Peyton, Diana Ensenat, Mohammed A. Azam, Amit N ... Arginase Promotes Neointima Formation in Rat Injured Carotid Arteries. Kelly J. Peyton, Diana Ensenat, Mohammed A. Azam, Amit N ...
Finally, neointima formation in a model of rat carotid artery balloon injury was significantly attenuated after treatment with ... These data demonstrate that LXR ligands inhibit VSMC proliferation and neointima formation after balloon injury and suggest ... Liver X receptor agonists suppress vascular smooth muscle cell proliferation and inhibit neointima formation in balloon-injured ...
BuMA OCT Study(A Comparative Evaluation of the Extent of Neointima Formation at 3 Months After Implantation Using OCT). The ... The objective of this study is a comparative evaluation of BuMA stent and of EXCEL stent in terms of the extent of neointima ... BuMA OCT Study(A Comparative Evaluation of BuMA Stent and of EXCEL Stent in Terms of the Extent of Neointima Formation at 3 ... Neointima. Cardiovascular Diseases. Pathologic Processes. Chest Pain. Pain. Neurologic Manifestations. Nervous System Diseases ...
... mm2 and of the neointima 1.34 (0.08) mm2. The thickness of the neointima at each strut was 0.17 (0.01) mm. ... The quantity of neointima is directly proportional to the amount of injury inflicted upon the artery by the stent itself.1 That ... Gunn J, Arnold N, Chan KH, et al. Coronary artery stretch versus deep injury in the development of in-stent neointima. Heart ... We have shown that stent induced stretch of coronary arteries results in a neointima whose magnitude is directly related to a ...
Role of kinins and nitric oxide in the effects of ACE inhibition on neointima formation. Circ Res. 1993;72:1202-1210. ... Inhibition of neointima formation in rat carotid artery after adenovirus-mediated kallikrein gene delivery. A through D show ... Smooth-muscle-cell proliferation and differentiation in neointima formation and vascular restenosis. Clin Sci. 1994;87:467-479. ... The lumen, neointima, media areas were measured by use of the NIH Image 1.60 software package. ...
However, the role of IRF3 in vascular neo-intima formation is unknown. We evaluated the protective role of IRF3 against neo- ... Global knockout of IRF3 (IRF3-KO) led to accelerated neo-intima formation and proliferation of VSMCs, whereas the opposite was ... Vascular smooth muscle cell (VSMC) proliferation is central to the pathophysiology of neo-intima formation. Interferon ... IRF3 inhibits VSMC proliferation and neo-intima formation after vascular injury through PPARγ activation. ...
We present TRPC6 as an actionable target to prevent neointima formation secondary to vascular injury and stent implantation. ... A proteomic atlas of the neointima identifies novel druggable targets for preventive therapy.. ... While Trpc6-/- mice presented reduced neointima formation compared to wild-type mice (1.44 ± 0.39 vs. 2.16 ± 0.48, P = 0.01), ... Here, we sought to investigate the molecular processes underlying neointima formation and to identify new treatment and ...
Neointima. Specific binding of [125I-Tyr0]CNP-(1-22) occurred throughout the neointima but tended to be most concentrated near ... Development of Neointima. The neointima developed as originally described27 for this preparation. Control arteries had no cells ... occurred in 7-day neointima, and 34±10/mm2 were present in neointima at 20 days (Fig 1⇓). ... NPR-C-like receptors also occur on the neointima. These findings are important because both NPR-B6 7 8 and NPR-C-like receptors ...
Characterization of the neointima revealed that WT (n=8) and Csrp2−/− (n=8) neointima had similar cell densities (19.6±0.5 and ... Increased Neointima Formation in Cysteine-Rich Protein 2-Deficient Mice in Response to Vascular Injury. Jiao Wei, Terri E. ... In Csrp2−/− mice (n=9) (Figure 6F), we observed 7.1±2.7% of BrdUrd incorporation in the neointima (P=0.63 versus WT) and 6.0± ... The cells observed in the neointima at the 4-day time point might reflect migrated rather than proliferating cells.6,7 En face ...
Core2 1-6-N-glucosaminyltransferase-I deficiency protects injured arteries from neointima formation in ApoE-deficient mice. - ... Arterial neointima induced by wire injury was smaller in C2GlcNAcT-I-deficient apoE(-/-) mice than in control apoE(-/-) mice (a ... Core2 1-6-N-glucosaminyltransferase-I deficiency protects injured arteries from neointima formation in ApoE-deficient mice.. ... C2GlcNAcT-I deficiency suppresses injury-induced arterial neointima formation, and this effect is attributable to decreased ...
We studied which of the events leading to neointima formation are involved in the effects of ACEI ... decrease neointima formation, and a kinin receptor antagonist partially reverses this inhibitory effect. ... 2) in the neointima, and this effect was abolished by cotreatment with icatibant (P < 0.05).ConclusionThe ACEI needs to be ... We studied which of the events leading to neointima formation are involved in the effects of ACEI and kinins.MethodsWe ...
2-Methoxyestradiol, an estradiol metabolite, inhibits neointima formation and smooth muscle cell growth via double blockade of ... Download PDF 2-Methoxyestradiol, an estradiol metabolite, inhibits neointima formation and smooth muscle cell growth via ... In rats, treatment with 2-ME abrogated injury-induced neointima formation; decreased proliferating SMCs; downregulated ... In rats, treatment with 2-ME abrogated injury-induced neointima formation; decreased proliferating SMCs; downregulated ...
Endovascular procedures cause transient endothelial injury but do not disrupt mature neointima in Drug Eluting Stents. ... Imaging of in-stent neointima at 28 days after stent placement did not lead to neointimal rupture. Guidewire, IVUS and OCT ... Endovascular procedures cause transient endothelial injury but do not disrupt mature neointima in Drug Eluting Stents. ...
Arterial thrombosis, neointima formation, and re-endothelialization were studied in a murine carotid artery injury model. ... Arterial thrombosis, neointima formation, and re-endothelialization were studied in a murine carotid artery injury model. ... Download PDF PI3K/p110α inhibition selectively interferes with arterial thrombosis and neointima formation, but not re- ... PI3K/p110α inhibition selectively interferes with arterial thrombosis and neointima formation, but not re-endothelialization: ...
MOBILIZATION OF ENDOTHELIAL PROGENITOR CELLS AND NEOINTIMA FORMATION AFTER IMPLANTATION OF EPC-CAPTURE STENTS IN NSTE-ACS (JACK ... MOBILIZATION OF ENDOTHELIAL PROGENITOR CELLS AND NEOINTIMA FORMATION AFTER IMPLANTATION OF EPC-CAPTURE STENTS IN NSTE-ACS (JACK ... MOBILIZATION OF ENDOTHELIAL PROGENITOR CELLS AND NEOINTIMA FORMATION AFTER IMPLANTATION OF EPC-CAPTURE STENTS IN NSTE-ACS (JACK ...
miRNA-21 is dysregulated in response to vein grafting in multiple models and genetic ablation in mice attenuates neointima ... miRNA-21 is dysregulated in response to vein grafting in multiple models and genetic ablation in mice attenuates neointima ... miRNA-21 is dysregulated in response to vein grafting in multiple models and genetic ablation in mice attenuates neointima ... miRNA-21 is dysregulated in response to vein grafting in multiple models and genetic ablation in mice attenuates neointima ...
PAR-2 mediates increased inflammatory cell adhesion and neointima formation following vascular injury in the mouse ... Since adhesion of leukocytes is increased following vascular injury and is important in determining the extent of neointima ... protease activated receptor-2 (PAR-2), lymphocyte, vascular injury, adhesion, neointima, pharmacology, Therapeutics. ... PAR-2 mediates increased inflammatory cell adhesion and neointima formation following vascular injury in the mouse. ...
neointima, farnesyl transferase inhibitor, arteries, angioplasty, Pharmacy and materia medica, Cardiology and Cardiovascular ... Short-term local delivery of an inhibitor of ras farnesyltransferase prevents neointima formation in vivo after porcine ... it can inhibit neointima formation. Methods and Results- FPTIII (1 to 25 µmol/L) concentration-dependently reduced p21ras ... Application of 25 µmol/L FPTIII locally for 15 minutes to balloon-injured porcine coronary arteries in vivo prevented neointima ...
  • While Trpc6-/- mice presented reduced neointima formation compared to wild-type mice (1.44 ± 0.39 vs. 2.16 ± 0.48, P = 0.01), activating or repressing TRPC6 in human vascular smooth muscle cells resulted in increased [vehicle 156.9 ± 15.8 vs. 1-oleoyl-2-acetyl-sn-glycerol 179.1 ± 8.07 (103 pixels), P = 0.01] or decreased migratory capacity [vehicle 130.0 ± 26.1 vs. SAR7334 111.4 ± 38.0 (103 pixels), P = 0.04], respectively. (onmedica.com)
  • Since adhesion of leukocytes is increased following vascular injury and is important in determining the extent of neointima formation, we hypothesised that mice lacking PAR-2 may have reduced neointima formation following vascular injury. (strath.ac.uk)
  • Paclitaxel-eluting stents reduced neointima formation (0.423 ± 0.065 vs. 0.240 ± 0.040 mm(2), P = 0.038), but decreased endothelial cell repopulation (238 ± 17 vs. 154 ± 22 nuclei/mm(2), P = 0.018), despite complete strut coverage. (ox.ac.uk)
  • In contrast to paclitaxel-eluting stents, reduced neointima formation in GCH-Tg mice was accompanied by increased endothelial cell coverage (156 ± 17 vs. 209 ± 23 nuclei/mm(2), P = 0.043). (ox.ac.uk)
  • Animals treated with cilazapril (10 mg/kg/day) had markedly reduced neointima formation, but in animals receiving infusion of Ang II, treatment with cilazapril did not suppress development of neointimal lesions. (elsevier.com)
  • In addition, apocynin significantly reduced neointima formation and proliferation of cells in both the neointima and adventitia. (edu.au)
  • Liver X receptor agonists suppress vascular smooth muscle cell proliferation and inhibit neointima formation in balloon-injured rat carotid arteries. (nih.gov)
  • 5 Specific Ang II receptor antagonists can also partially inhibit neointima formation, which suggests that the inhibition of neointima formation by ACE inhibitors is, in part, because of a decreased level of Ang II. (ahajournals.org)
  • Our aim was to demonstrate in biochemical studies that farnesyl protein transferase inhibitor III (FPTIII) is an inhibitor of p21ras processing and that when it is given locally in vivo at the site of coronary balloon injury in a porcine model, it can inhibit neointima formation. (strath.ac.uk)
  • Scope: Curcumin has been shown to affect platelet-derived growth factor (PDGF)- and tumor necrosis factor (TNF)-α-elicited vascular smooth muscle cell (VSMC) migration and inhibit neointima formation following vascular injury. (elsevier.com)
  • Objective: The aim of this study was to determine the roles of AMPK alpha in the development of vascular neointima hyperplasia and to elucidate the underlying mechanisms. (rti.org)
  • To investigate the effect of Sirolimus on vein graft neointima hyperplasia via oral administration compared with local delivery, and find out an effective and safe way to provide support for clinical application. (bvsalud.org)
  • Compared with blank- control group , neointima hyperplasia was inhibited significantly in group 3 and group 4 intima thickness were (90.11?10.99)?m versus (29.38?10.45) ?m, (18.29?9.03)?m, respectively. (bvsalud.org)
  • CONCLUSIONS: NADPH oxidase is implicated in vascular remodelling and superoxide-stimulated cell proliferation in the neointima contributes to intimal hyperplasia in this collar model. (edu.au)
  • The result of these vascular events is intimal hyperplasia, whereby vascular smooth muscle cells (VSMCs) migrate from the media to the intima, proliferate, and consequently, form the neointima. (aspetjournals.org)
  • CD9 is upregulated in senescent endothelial cells, neointima hyperplasia, and atherosclerotic plaques. (nature.com)
  • Neointima hyperplasia was minimal in the single-PED-group animals. (ajnr.org)
  • Methods and Results- Balloon injury of rat carotid arteries resulted in a sustained increase in arginase activity in the vessel wall and the induction of arginase I protein in both the media and neointima of injured vessels. (ahajournals.org)
  • Objective In balloon-injured rat carotid arteries, angiotensin-converting enzyme inhibitors (ACEI) decrease neointima formation, and a kinin receptor antagonist partially reverses this inhibitory effect. (ovid.com)
  • When introduced locally to balloon-injured rat carotid arteries, a well characterized model of a VSMC-derived lesion, Ad-FasL functioned as a potent inhibitor of neointima formation. (scienceexchange.com)
  • Local delivery of platelets with encapsulated iloprost to balloon injured pig carotid arteries: effect on platelet deposition and neointima formation. (ox.ac.uk)
  • Western blotting analysis revealed that both cathepsin S and K protein levels also increased in the carotid arteries during neointima formation, coinciding with an increase elastolytic activity assayed using Elastin-Congo red, whereas, no significant change in the expressions of cystatin C mRNA and protein was observed during follow-up periods after injury. (elsevier.com)
  • C1-esterase inhibitor protects against neointima formation after arterial injury in atherosclerosis-prone mice. (nih.gov)
  • Finally, neointima formation after mechanical arterial injury was increased in AMPK alpha 2(-/-) but not AMPK alpha 1(-/-) mice. (rti.org)
  • Core2 1-6-N-glucosaminyltransferase-I deficiency protects injured arteries from neointima formation in ApoE-deficient mice. (curehunter.com)
  • Arterial neointima induced by wire injury was smaller in C2GlcNAcT-I-deficient apoE (-/-) mice than in control apoE (-/-) mice (a 79% reduction in size). (curehunter.com)
  • PF4 deficiency accelerated endothelial regeneration and protected mice from neointima formation after arterial injury. (curehunter.com)
  • Our data show that PAR-2 modulates inflammatory cell adhesion when stimulated and in mice lacking the PAR-2 receptor, adhesion to injured vessels is reduced with a consequent reduction in neointima formation. (strath.ac.uk)
  • Histological examination revealed that the neointima is markedly thickened in A2bAR KO mice compared with WT mice. (pnas.org)
  • METHODS AND RESULTS: Endothelial cell repopulation was assessed en face in stented arteries in ApoE(-/-) mice with endothelial-specific LacZ expression. (ox.ac.uk)
  • GCH-Tg ApoE(-/-) mice had less neointima formation compared with ApoE(-/-) littermates (0.52 ± 0.08 vs. 0.26 ± 0.09 mm(2), P = 0.039). (ox.ac.uk)
  • Neointima formation was investigated after vascular injury in FSAP -/- mice. (cdc.gov)
  • Objectives To determine whether neointima formation after vascular injury is increased in FSAP -/- mice. (cdc.gov)
  • Irisin treatment (0.5 μg/g body weight/day) significantly reduced the severity of aortic atherosclerosis in apolipoprotein E-deficient mice fed on a high-cholesterol diet and suppressed carotid neointima formation in a carotid partial ligation model. (plos.org)
  • The aims of this work were to determine if aPLs directly promote medial hypertrophy or neointima formation in mice and to identify the underlying mechanisms. (elsevier.com)
  • Methods and Results-Medial hypertrophy and neointima formation invoked by carotid artery endothelial denudation were evaluated in mice administered normal human IgG or aPLs. (elsevier.com)
  • Conclusions-APLs blunt endothelial repair, and there is related aPL-induced exaggeration in neointima formation after endothelial injury in mice. (elsevier.com)
  • Finally, CARD9-KO decreased neointima formation of grafted veins in mice. (elsevier.com)
  • Soluble epoxide hydrolase deficiency attenuates neointima formation in the femoral cuff model of hyperlipidemic mice. (qxmd.com)
  • Effect of sinomenine on vascular smooth muscle cell dedifferentiation and neointima formation after vascular injury in mice. (qxmd.com)
  • Figure 2: SRSF1 deficiency in VSMCs inhibits neointima formation. (nature.com)
  • Here we studied the intracellular mechanisms by which 2-ME inhibits SMC growth and whether 2-ME prevents injury-induced neointima formation. (uzh.ch)
  • Adenovirus-mediated over-expression of the cyclin/cyclin-dependent kinase inhibitor, p21 inhibits vascular smooth muscle cell proliferation and neointima formation in the rat carotid artery model of balloon angioplasty. (semanticscholar.org)
  • Fas ligand gene transfer to the vessel wall inhibits neointima formation and overrides the adenovirus-mediated T cell response. (scienceexchange.com)
  • 3,3'Diindolylmethane suppresses vascular smooth muscle cell phenotypic modulation and inhibits neointima formation after carotid injury. (qxmd.com)
  • We hypothesize that sEH in VSMCs plays a pivotal role in atherosclerosis and injury-induced neointima formation. (qxmd.com)
  • Progressive atherosclerosis within the neointima is an another possible cause of LST, but this phenomenon has seldom been reported in DES. (bvsalud.org)
  • Although multiple factors contributing to late stent failure have been proposed, de novo development of atherosclerosis within the neointima has been identified as a major cause [ 5 , 6 ]. (hindawi.com)
  • Aims Inflammation plays an important role in the neointima formation of grafted veins. (elsevier.com)
  • The pre-operative lipid phenotype plays a marginal role in the neointima formation. (cdc.gov)
  • Endothelial cell repopulation after stenting determines in-stent neointima formation: effects of bare-metal vs. drug-eluting stents and genetic endothelial cell modification. (ox.ac.uk)
  • CONCLUSION: Drug-eluting stents reduce not only neointima formation but also endothelial cell repopulation, independent of strut coverage. (ox.ac.uk)
  • However, the exact mechanism and mediators responsible for VSMC activation and neointima formation after injury of the vessel wall remain elusive. (ahajournals.org)
  • These data demonstrate that LXR ligands inhibit VSMC proliferation and neointima formation after balloon injury and suggest that LXR ligands may constitute a novel therapy for proliferative vascular diseases. (nih.gov)
  • However, an absence of CRP2 enhanced VSMC migration and increased neointima formation following arterial injury. (ahajournals.org)
  • CONCLUSIONS: We conclude that TRAIL induction involves FGF-2, Sp1-phosphorylation and NFκB and that TRAIL promotes VSMC proliferation and neointima formation after arterial injury. (sahmriresearch.org)
  • We aimed to evaluate the effects and characterize the molecular mechanisms of DMC on VSMC migration and neointima formation in a carotid injury model. (elsevier.com)
  • Bone marrow-derived progenitor cells (BMPCs) as well as perivascular progenitor cells have been implicated to differentiate into vascular cells during neointima formation. (ahajournals.org)
  • Neointima formation occurs frequently after angioplasty and causes significant morbidity;vascular smooth muscle cells (SMCs) are key cells during neointima formation. (grantome.com)
  • We also plan to study the role of PPAR3 activation specifically in smooth muscle cells during neointima formation. (grantome.com)
  • Results: Both rate and degree of neointima formation increase dramatically with overexpression (250%-461% relative to controls at 7 and 28 days). (elsevier.com)
  • Systemic infusion, although significant, did not attain the degree of neointima formation present with overexpression. (elsevier.com)
  • Common hepatic lipase gene promoter variant predicts the degree of neointima formation after carotid endarterectomy: impact of plaque composition a. (cdc.gov)
  • The objective of this study is a comparative evaluation of BuMA stent and of EXCEL stent in terms of the extent of neointima formation at 3 months after implantation using OCT. (clinicaltrials.gov)
  • We studied which of the events leading to neointima formation are involved in the effects of ACEI and kinins. (ovid.com)
  • C1 esterase inhibitor protects against neointima formation aft. (nih.gov)
  • 4 Angiotensin-converting enzyme (ACE) inhibitor suppresses neointima formation after endothelial injury in rat carotid artery and abdominal aorta. (ahajournals.org)
  • We have now examined the action of the NADPH oxidase inhibitor apocynin, given via the adventitia, on the neointima formation and endothelial function in this model. (edu.au)
  • In vivo, the sEH inhibitor led to a significant decrease in injury-induced neointima formation in a rat carotid-artery injury model. (qxmd.com)
  • Restenosis is caused by growth of a neointima, comprised of smooth muscle cells and intercellular matrix. (bmj.com)
  • Therefore, we propose a method for neointima restenosis quantification after stent implantation, thereby providing information to potential treatments. (usp.br)
  • Experimental injury of the rat aorta causes rapid migration of medial smooth muscle cells and their proliferation resulting in the formation of neointima. (jci.org)
  • We have examined, using quantitative autoradiography, the expression of angiotensin II receptor subtypes AT1 and AT2, and angiotensin-converting enzyme, in the neointima formed in the rat thoracic aorta 15 d after balloon-catheter injury. (jci.org)
  • Whether AMPK alpha alters vascular neointima formation induced by vascular injury is unknown. (rti.org)
  • This study investigated the impact of arginase on cell cycle progression and neointima formation after experimental arterial injury. (ahajournals.org)
  • Furthermore, local perivascular application of the potent and selective arginase inhibitors S -(2-boronoethyl)- l -cysteine (BEC) or N G -hydroxy-nor- l -arginine (L-OHNA) immediately after injury markedly attenuated medial and neointimal DNA synthesis and neointima formation. (ahajournals.org)
  • Finally, neointima formation in a model of rat carotid artery balloon injury was significantly attenuated after treatment with the LXR ligand T1317 compared with vehicle-treated animals. (nih.gov)
  • The quantity of neointima is directly proportional to the amount of injury inflicted upon the artery by the stent itself. (bmj.com)
  • We have previously shown that stretch is ubiquitous after stenting and, even in the absence of deep injury, is an important mediator of neointima formation. (bmj.com)
  • Therefore, in this study, we aimed to examine the contribution of a wide panel of parameters of stent geometry to the development of neointima in stent sections that displayed stretch but not deep injury. (bmj.com)
  • Here, we sought to investigate the molecular processes underlying neointima formation and to identify new treatment and prevention targets.Neointima formation was induced by wire injury in mouse femoral arteries. (onmedica.com)
  • We present TRPC6 as an actionable target to prevent neointima formation secondary to vascular injury and stent implantation. (onmedica.com)
  • Thus, whereas levels of NPR-B did not change significantly after arterial injury and NPR-A was not detected, NPR-C-like receptors were unregulated as mitosis declined in the media and as a prominent neointima formed. (ahajournals.org)
  • C2GlcNAcT-I deficiency suppresses injury-induced arterial neointima formation , and this effect is attributable to decreased leukocyte recruitment to injured vascular walls and increased endothelial regeneration. (curehunter.com)
  • Methods We administered 5 mg/kg per day ramipril, either alone or combined with the kinin receptor antagonist icatibant (Hoe 140), on the days each wave occurred and studied the effects on neointima formation 14 days after balloon injury. (ovid.com)
  • Ramipril alone or combined with icatibant had no effect on neointima formation when administered from 2 days before to 3 or 5 days after balloon injury. (ovid.com)
  • Arterial thrombosis, neointima formation, and re-endothelialization were studied in a murine carotid artery injury model. (uzh.ch)
  • In line with this observation, treatment with PIK75 selectively inhibited neointima formation without affecting re-endothelialization following vascular injury. (uzh.ch)
  • CONCLUSION: Following vascular injury, PI3K/p110α inhibition selectively interferes with arterial thrombosis and neointima formation, but not re-endothelialization. (uzh.ch)
  • Conclusions-These results show that increased expression of MT-MMP-1 and activation of MMP-2 occurs early after injury to the rat carotid artery and that at later times MMP-2 is preferentially localized to the developing neointima. (elsevier.com)
  • In Aim Three, we will determine which agent can reduce neointima size the greatest after wire injury. (grantome.com)
  • Angiotensin converting enzyme inhibition markedly suppresses neointima formation in response to balloon catheter-induced vascular injury of the rat carotid artery. (elsevier.com)
  • Animals that received continuous infusion of Ang II (0.3 μg/min/rat) were found to have significantly greater neointima formation in response to balloon injury than controls. (elsevier.com)
  • These data support the conclusions that converting enzyme inhibition prevents neointima formation after vascular injury through inhibition of Ang II generation. (elsevier.com)
  • Supplementary MaterialsFigure S1: Vinpocetine will not affect apoptosis in neointima following balloon injury in vivo. (healthyfutureforkids.com)
  • Inhibition of endothelial progenitor cell glycogen synthase kinase-3beta results in attenuated neointima formation and enhanced re-endothelialization after arterial injury. (qxmd.com)
  • This concept may have clinical ramifications given that factors which enhance interstitial flow (i.e., chemical or mechanical injury to the endothelium and inflammation and hypertension induced enhancement of vascular permeability) are associated with vessel remodeling and neointima formation. (semanticscholar.org)
  • Maladaptive remodelling of the arterial wall after mechanical injury (e. g. angioplasty) is characterised by inflammation, neointima formation and media hypertrophy, resulting in narrowing of the affected artery. (nih.gov)
  • MK2-deficiency (ldlr-/-/mk2-/-) nearly completely prevented neointima formation, media hypertrophy, and lumen loss after injury. (nih.gov)
  • Neointima can form as a result of vascular surgery such as angioplasty or stent placement. (wikipedia.org)
  • Balloon angioplasty enhances the expression of angiotensin II AT1 receptors in neointima of rat aorta. (jci.org)
  • The lumen enlargement after balloon angioplasty is the combined effect of further stent expansion and extrusion-axial redistribution of the neointima. (bmj.com)
  • Conclusion: With some evidence of dose-dependence, tissue plasminogen activator enhances neointima formation after angioplasty in a rabbit model. (elsevier.com)
  • We have studied the effects of autologous platelets, electroloaded with the stable prostacyclin analogue, iloprost on platelet deposition and neointima formation in a pig carotid angioplasty model. (ox.ac.uk)
  • Acute platelet deposition was measured using 111-Indium, and neointima formation at 21 days post angioplasty was assessed by morphometric analysis. (ox.ac.uk)
  • In conclusion, we provide evidence that BMPCs within the neointima rarely co-express markers for vascular cells and do not contribute to the neointimal cellular mass beyond the inflammatory response. (ahajournals.org)
  • For each section (n = 99), with its associated neointimal and luminal areas, we measured the number of struts, percentage metal coverage of the arterial wall, stent major and minor axes, stent oblateness, and areas of the lumen and the neointima. (bmj.com)
  • Imaging of in-stent neointima at 28 days after stent placement did not lead to neointimal rupture. (eur.nl)
  • In contrast, selective targeting of endothelial cell function is sufficient to improve endothelial cell repopulation and reduce neointima formation. (ox.ac.uk)
  • Our hypothesis is that PPAR3 activation specifically in smooth muscle cells (SMC) will reduce neointima formation by decreasing resident SMC migration and proliferation as well as SMC-derived chemokine production and subsequent recruitment of bone marrow-derived cells. (grantome.com)
  • Factor VII-activating protease deficiency promotes neointima formation by enhancing leukocyte accumulation. (cdc.gov)
  • Targeting endothelial cell function is a rational therapeutic strategy to improve vascular healing and decrease neointima formation after stenting. (ox.ac.uk)
  • Apigenin attenuates neointima formation via suppression of vascular smooth muscle cell phenotypic transformation. (qxmd.com)
  • A2bAR Deficiency Enhances Postinjury Neointima Formation in the Vasculature. (pnas.org)
  • Interestingly, an in vivo model of smooth muscle cell proliferation revealed that an A2 receptor agonist, 2-octynyladenosine, inhibited neointima formation ( 8 ). (pnas.org)
  • immunocytochemistry and Western blotting showed that the increase occurred preferentially in the developing neointima. (elsevier.com)
  • Immunohistochemistry, Western blot, and in situ hybridization showed that the increase of cathepins S and K and the decrease of cystatin C occurred preferentially in the developing neointima. (elsevier.com)
  • Lack of angiogenic factors in the vascular graft wall may cause for unhealing neointima. (nii.ac.jp)
  • The capabilities of OCT are well suited for the identification of calcified plaque and neointima formation after stent implantation. (springer.com)
  • Stent implantation under low flow is associated with increased neointima formation. (uthscsa.edu)
  • FPTIII also prevented p42/p44 MAPK activation and DNA synthesis in response to platelet-derived growth factor in these cells at a concentration of 25 µmol/L. Application of 25 µmol/L FPTIII locally for 15 minutes to balloon-injured porcine coronary arteries in vivo prevented neointima formation assessed at 4 weeks, reduced proteoglycan deposition, and inhibited adventitial hypertrophy. (strath.ac.uk)
  • FPTIII also prevented p42/p44 MAPK activation and DNA synthesis in response to platelet-derived growth factor in these cells at a concentration of 25 μmol/L. Application of 25 μmol/L FPTIII locally for 15 minutes to balloon-injured porcine coronary arteries in vivo prevented neointima formation assessed at 4 weeks, reduced proteoglycan deposition, and inhibited adventitial hypertrophy. (gla.ac.uk)
  • We use either local adenoviral-mediated overexpression of tPA or systemic infusion of recombinant tPA combined with mechanical overdilation of rabbit common femoral arteries to evaluate the impact of tPA on neointima formation. (elsevier.com)
  • ADAMTS-7 mediates vascular smooth muscle cell migration and neointima formation in balloon-injured rat arteries. (qxmd.com)
  • Conclusion The innate immune protein CARD9 in macrophages may mediate necrotic SMC-induced inflammation by activating NF-κB and contributed to neointima formation in the vein grafts. (elsevier.com)
  • Further experiments showed that aPL antagonism of endothelial migration and repair is mediated by antibody recognition of β2-glycoprotein I, apolipoprotein E receptor 2, and a decline in bioavailable NO. Consistent with these mechanisms, the adverse impacts of aPLs on reendothelialization and neointima formation were fully prevented by the NO donor molsidomine. (elsevier.com)
  • While aPLs had no effect on medial hypertrophy, they caused exaggerated neointima development. (elsevier.com)
  • Mindin regulates vascular smooth muscle cell phenotype and prevents neointima formation. (qxmd.com)
  • External supports and the prevention of neointima formation in vein grafts. (ox.ac.uk)
  • AIMS AND METHODOLOGY: the aim of this review is to provide an overview of the aetiology of neointima formation in vein grafts and to highlight the use of an external support to modulate this phenomenon. (ox.ac.uk)
  • The increase in local kinin accumulation may also be involved in the inhibition of neointima formation because icatibant, a bradykinin B 2 receptor antagonist, can partially block the protective effect of ACE inhibitors. (ahajournals.org)
  • Example for neointima formation in a female rabbit aortic section after endothelial balloon denudation and 21 days of cultivation in medium containing 1 % isopropanol and 1 % DMSO. (biomedcentral.com)
  • Vascular smooth muscle cells are stained in the medial tissue and in the neointima. (biomedcentral.com)
  • Severe medial tear was associated with exuberant neointima. (medscape.com)
  • Each independent parameter (stent geometry) was tested for significance against each dependent parameter (lumen and neointima areas and thicknesses) to yield a list of stent geometry parameters that correlated with arterial morphometry. (bmj.com)
  • Curcumin significantly attenuates carotid artery neointima formation. (greenmedinfo.com)
  • The LIPC promoter -514 C-T polymorphism is associated with a significantly reduced development of neointima after surgery. (cdc.gov)
  • Neointima, which became evident 5 to 7 days after arterial damage, expressed NPR-C-like sites and no detectable NPR-B-like binding. (ahajournals.org)
  • Neointima typically refers to scar tissue that forms within tubular anatomical structures such as blood vessels, as the intima is the innermost lining of these structures. (wikipedia.org)