Apolipoprotein A-IV is a member of the apo A-I/C-III/A-IV gene cluster. In order to investigate its hypothetical coordinated regulation, an acute phase was induced in pigs by turpentine oil injection. The hepatic expression of the gene cluster as well as the plasma levels of apolipoproteins were monitored at different time periods. Furthermore, the involvement of the inflammatory mediators interleukins 1 and 6 and tumor necrosis factor in the regulation of this gene cluster was tested in cultured pig hepatocytes, incubated with those mediators and apo A-I/C-III/A-IV gene cluster expression at the mRNA level was measured. In response to turpentine oil-induced inflammation, a decreased hepatic apo A-IV mRNA expression was observed (independent of apo A-I and apo C-III mRNA) not correlating with the plasma protein levels. The distribution of plasma apo A-IV experienced a shift from HDL to larger particles. In contrast, the changes in apo A-I and apo C-III mRNA were reflected in their corresponding plasma
Background: Apolipoprotein C-III (apoC-III) inhibits lipoprotein lipase activity and hepatic uptake of triglyceride-rich lipoproteins. Elevated levels of apoC-III have been found to be an independent predictor for CHD risk and genetically reduced apoC-III is associated with protection from CHD, making apoC-III a therapeutic target. Omega-3 fatty acid formulations containing docosahexaenoic acid (DHA) have been shown to increase LDL-C in patients with severe hypertriglyceridemia (HTG). Clinical data suggest that eicosapentaenoic acid (EPA) alone, which lowers triglycerides to a similar extent as EPA + DHA, does not raise LDL-C, but also fails to lower apoC-III. Materials: The EVOLVE trial evaluated 2, 3, and 4 g/d of a novel omega-3 free-fatty acid (FFA) formulation containing both EPA + DHA compared with 4 g/d of olive oil. In 399 patients with severe HTG we evaluated the effects on plasma apoC-III levels and the correlations between change in apoC-III and change in plasma lipids (TG, LDL-C) ...
We provide new information on the dose-ranging effect of rosuvastatin, a potent HMG-CoA (or 3-hydroxy-3-methyl-glutaryl-CoA) reductase inhibitor, on VLDL apoC-III metabolism in subjects with the metabolic syndrome. We demonstrated that rosuvastatin dose-dependently decreased VLDL apoC-III concentrations by increasing the FCR and decreasing the PR of VLDL apoC-III. These results add further to our work on the dose-dependent effect of rosuvastatin on apoB-containing lipoproteins and HDL particle kinetics in the same subjects (13,14).. Hypertriglyceridemia in insulin-resistant states, including the metabolic syndrome, results from overproduction and reduced catabolism of TRL and their remnants. These kinetic aberrations may be related to altered VLDL apoC-III metabolism. Previous studies demonstrated that overproduction of VLDL apoC-III explained the higher VLDL apoC-III concentration in these subjects (17). The increased VLDL apoC-III concentration and production rate were associated with elevated ...
Apolipoprotein CIII (apoCIII) is an independent risk for coronary heart disease (CHD). In this study, we investigated the associations among plasma apoCIII, hs-CRP and TNF-α levels and their roles in the clinical features of CHD in the Li and Han ethnic groups in China. A cohort of 474 participants was recruited (238 atherosclerotic patients and 236 healthy controls) from the Li and Han ethnic groups. Blood samples were obtained to evaluate apoCIII, TNF-α, hs-CRP and lipid profiles. Chi-squared, t-tests, and Kruskal-Wallis or Wilcoxon-Mann-Whitney tests, Pearson or Spearman correlation tests and multiple unconditional logistic regression were employed to analyze lipid profiles and variations in plasma apoCIII, TNF-α, hs-CRP in subgroups of CHD and their contributions to CHD using SPSS version 20.0 software. Compared to healthy participants, unfavorable lipid profiles were identified in CHD patients with enhanced systolic pressure, diastolic pressure, fasting blood sugar (FBS), TG, TC, LDL-C, apoB, Lp
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RAPOSO, HELENA F.... Apolipoprotein CIII overexpression exacerbates diet-induced obesity due to adipose tissue higher exogenous lipid uptake and retention and lower lipolysis rates. NUTRITION & METABOLISM 12 n. p. DEC 23 2015. Journal article.
C H Bolton, A P Corfield, L G Downs; Sialidase Activity Acting on Apolipoprotein CIII 1 and 2 in Human Leukocytes and Platelets. Clin Sci (Lond) 1 January 1984; 67 (s9): 15P. doi: https://doi.org/10.1042/cs067015P. Download citation file:. ...
Recent development in gene targeting tools makes production of knockout (KO) rabbits possible. In the present work, we generated five...
C2C12 myotubes exposed to VLDL showed increased levels of ER stress and inflammatory markers whereas peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α) and AMP-activated protein kinase (AMPK) levels were reduced and the insulin signalling pathway was attenuated. The effects of VLDL were also observed in isolated skeletal muscle incubated with VLDL. The changes caused by VLDL were dependent on extracellular signal-regulated kinase (ERK) 1/2 since they were prevented by the ERK1/2 inhibitor U0126 or by knockdown of this kinase by siRNA transfection. ApoCIII mimicked the effects of VLDL and its effects were also blocked by ERK1/2 inhibition, suggesting that this apolipoprotein was responsible for the effects of VLDL. Skeletal muscle from transgenic mice overexpressing apoCIII showed increased levels of some ER stress and inflammatory markers and increased phosphorylated ERK1/2 levels, whereas PGC-1α levels were reduced, confirming apoCIII effects in vivo. Finally, incubation ...
Results A higher triglyceride/cholesterol ratio of LDL was found more in HCV-infected donors than in healthy volunteers, and the triglyceride/cholesterol ratio of LDL-LVP was much increased, suggesting that the LPL hydrolysis of triglyceride may be impaired. VLDL, VLDL-LVP, LDL-LVP, but not LDL, suppressed LPL lipolytic activity, which was restored by antibodies that recognised apoC-III/-IV and correlated with the steadily abundant apoC-III/-IV quantities in those particles. In a cell-based system, treatment with VLDL and LVPs reversed the LPL-mediated inhibition of HCV infection in apoC-III/-IV-dependent manners. A multivariate logistic regression revealed that plasma HCV viral loads correlated negatively with LPL lipolytic activity, but positively with the apoC-III content of VLDL. Additionally, apoC-III in VLDL was associated with a higher proportion of HCV-RNA than was IgG.. ...
Jianglin Fan is the author of this article in the Journal of Visualized Experiments: Production of Apolipoprotein C-III Knockout Rabbits using Zinc Finger Nucleases
The authors of the following article have requested that it be retracted from publication in Circulation Research:. Kawakami A, Osaka M, Aikawa M, Uematsu S, Akira S, Libby P, Shimokado K, Sacks FM, Yoshida M. Toll-like receptor 2 mediates apolipoprotein CIII-induced monocyte activation. Circ Res. 2008;103:1402-1409.. The corresponding author, Dr Akio Kawakami, admitted to the editors to improperly handling the collection and presentation of data in this article such that the authors can no longer verify the authenticity and accuracy of the data presented. These errors include, but may not be limited to, the blots in Figure 2A, Figure 4D, and Online Figure III originating from unrelated experiments of the corresponding author, and the incorrect reporting of "n" in Figures 5 and 6, which are less than indicated. As such, data in those figures are not verifiable.. All co-authors involved in this study other than the corresponding author, Dr Kawakami, had no knowledge of any scientific impropriety ...
Rabbit polyclonal Apolipoprotein CIII antibody validated for WB, ELISA, ICC/IF, sELISA and tested in Human. Referenced in 3 publications. Immunogen…
Transcriptionally controlled transcription factor. Binds to DNA sites required for the transcription of alpha 1-antitrypsin, apolipoprotein CIII, transthyretin genes and HNF1-alpha. May be essential for development of the liver, kidney and intestine.
Ionis Pharmaceuticals, through its wholly owned subsidiary Akcea Therapeutics, is developing IONIS APOCIII LRx, a GalNAc3 conjugated antisense oligonucleotide
Added to this, both observational and genetic studies have been concordant in showing that remnant cholesterol (which includes intermediate-density lipoproteins, very-low-density lipoproteins, and chylomicron remnants, the products of the lipolytic degradation of triglyceride-rich lipoproteins produced by the liver and intestine) is causal for ischaemic heart disease 8. Genetic studies have also shown associations between different players in triglyceride metabolism, apolipoprotein CIII and the angiopoietins-like 3 and 4 (ANGPTL3, ANGPTL4) and coronary artery disease (9-11); the latest Focus report discusses recent data for ANGPTL3 inhibition. Moreover, given the pivotal role of peroxisome proliferator-activated receptor ? (PPAR?) in controlling the expression of a number of key genes in triglyceride and HDL metabolism, efforts have been directed to modulating the unique receptor-cofactor binding profile to improve the potency and selectivity of PPAR? ligands (the SPPARM? concept). The ...
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WELCOME to the 103rd Season of the TOK-cok, SING-song, FOOD-Loving, BBB-spreading & Cat-Loving thread! Earlier threads - EXPOSE yourself - I EXPOSE yourself - II EXPOSE yourself - III EXPOSE yourself - IV EXPOSE yourself - V EXPOSE yourself - VI
WELCOME to the 103rd Season of the TOK-cok, SING-song, FOOD-Loving, BBB-spreading & Cat-Loving thread! Earlier threads - EXPOSE yourself - I EXPOSE yourself - II EXPOSE yourself - III EXPOSE yourself - IV EXPOSE yourself - V EXPOSE yourself - VI
Another substance class on the rise in cardiovascular medicine are so-called anti-sense oligonucleotides, single strands of DNA or RNA binding complementary to a chosen mRNA sequence, thereby preventing protein translation. Besides a fascinating novel anti-coagulatory approach by inhibiting coagulation factor XI production, the biggest focus of this novel therapeutic approach lies on lipidology. Within this review we will highlight the current evidence on antisense therapy against apolipoprotein B, apolipoprotein A as well as apolipoprotein CIII, that are in very different stages of development, however, with some exciting early data.. Kurzfassung: Biologika begr nden eine neue Medikamentenklasse, werden biotechnologisch hergestellt und greifen gezielt in molekularbiologische Mechanismen ein. Lange Zeit eine Dom ne der H matologie, Onkologie sowie der Rheumatologie, treten monoklonale Antik rper als Therapeutika nun auch langsam in der Kardiologie ihren Siegeszug an. Neben dem schon seit mehr ...
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hazard ratio per 1 SD [HR/SD]: 1.40; 95% confidence interval [CI]: 1.17 to 1.67), apoC-III (HR/SD: 1.38; 95% CI: 1.17 to 1.63), and apoE (HR/SD: 1.31; 95% CI: 1.13 to 1.52). Associations were independent of high-density lipoprotein ...
View Ldlr/Ldlr Tg(APOC3)3707Bres/? involves: 129S7/SvEvBrd * C57BL/6J * CBA/J: phenotypes, images, diseases, and references.
Compare APOC1 ELISA Kits from Biorbyt from leading suppliers on Biocompare. View specifications, prices, citations, reviews, and more.
Apolipoprotein C-II deficiency (APOC2) Test Cost INR 30000.00 Surat Pune Jaipur Lucknow Kanpur Nagpur Visakhapatnam Indore Thane Bhopal Patna Vadodara Ghaziabad Ludhiana Coimbatore Madurai Meerut Ranchi Allahabad Trivandrum Pondicherry Mysore Aligarh best offer discount price
Distribution of apolipoprotein C-II mRNA and protein in the perinatal mouse lung. Mouse tissue sections are from saccular stage (A, B, H, GD 19.5; C, G, PN 0; I
Serum: Use a serum separator tube (SST) and allow samples to clot for two hours at room temperature or overnight at 4°C before centrifugation for 15 minutes at 1000 ×g. Remove serum and assay immediately or aliquot and store samples at -20°C or -80°C. Avoid repeated freeze-thaw cycles ...
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Apolipoprotein A-IV/ApoA4 Antibody Pair. Matched antibody pairs validated for ELISA or IP-Western Blot. Backed by our 100% Guarantee.
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APOC4 Antibody 16530-1-AP has been identified with IF, WB, ELISA. 16530-1-AP detected 17 kDa band in human plasma tissue with 1:200-1:1000 dilution...
Apolipoprotein C2 or apolipoprotein C-II is a protein that in humans is encoded by the APOC2 gene. secreted in plasma where it is a component of very low density lipoproteins and chylomicrons. This protein activates the enzyme lipoprotein lipase in capillaries,[5] which hydrolyzes triglycerides and thus provides free fatty acids for cells. Mutations in this gene cause hyperlipoproteinemia type IB, characterized by xanthomas, pancreatitis, and hepatosplenomegaly, but no increased risk for atherosclerosis. Lab tests will show elevated blood levels of triglycerides, cholesterol, and chylomicrons[6] ...
Apolipoproteins function as structural components of lipoprotein particles, cofactors for enzymes, and ligands for cell-surface receptors. Most of the apoliporoteins exhibit proteoforms, arising from single nucleotide polymorphisms (SNPs) and post-translational modifications such as glycosylation, oxidation, and sequence truncations. Reviewed here are recent studies correlating apolipoproteins proteoforms with the specific clinical measures of lipid metabolism and cardiometabolic risk. Targeted mass spectrometric immunoassays toward apolipoproteins A-I, A-II, and C-III were applied on large cross-sectional and longitudinal clinical cohorts. Several correlations were observed, including greater apolipoprotein A-I and A-II oxidation in patients with diabetes and cardiovascular disease, and a divergent apoC-III proteoforms association with plasma triglycerides, indicating significant differences in the metabolism of the individual apoC-III proteoforms. These are the first studies of their kind, correlating
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Mar 7, 2005. rich lipoproteins secreted from doxycycline-treated cells was larger. cept that these two key apolipoproteins may interact within the
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Apolipoprotein (apolipoprotein) je bílkovinná složka lipoproteinů. Apolipoproteinů existuje více druhů a jednotlivé typy se vyskytují v konkrétních lipoproteinech. Apolipoproteiny mají více funkcí, jsou strukturálně důležité, pomáhají transportu lipoproteinových částic, a dokonce mohou fungovat jako koenzymy některých enzymů ...
Aim: There remains high unmet medical need for therapies to treat cardio/metabolic diseases. We validated in human trials, a platform for reducing the synthesis of genes expressed in the liver. The platform utilizes a GalNAc ligand attached to the 3 end of the sense strand of an RNAi molecule to enable delivery specifically to the liver. Here we extend the platform to targets of interest in cardiovascular disease, including PCSK9, ANGPLT3 and ApoC3.. METHODS: Chemically modified siRNAs were designed and were screened for potency in vitro. pM active siRNA molecules were developed targeting PCSK9, ANGPLT3 and ApoC3. The siRNAs were tested in either rodents or in non-human primates (NHPs) for activity.. RESULTS: In NHPs a single dose of ALN-PCSsc at 6 mg/kg reduced PCSK9 levels up to 97% and LDL-C up to 67%. Moreover the nadir effect (without any rebound of LDL-C) lasted ,30 days indicating that once a month or longer dosing frequency in clinic should be supported. Multidose studies in NHP at ...
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Yunifiar M, Muhammad Qushai; Kotaki, Tomohiro; Witaningrum, Adiana Mutamsari; Khairunisa, Siti Qamariyah; Indriati, Dwi Wahyu; Meilani, Meilani; Yeheskiel, Tigor; Ueda, Shuhei; Nasronudin, Nasronudin; Kameoka, ...
Yunifiar M, Muhammad Qushai; Kotaki, Tomohiro; Witaningrum, Adiana Mutamsari; Khairunisa, Siti Qamariyah; Indriati, Dwi Wahyu; Meilani, Meilani; Yeheskiel, Tigor; Ueda, Shuhei; Nasronudin, Nasronudin; Kameoka, ...
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Hypertriglyceridemia is characterised by high levels of triglycerides in the blood and is associated with several metabolic disorders and with an increased risk of cardiovascular disease. It can be caused by several factors, including obesity, excessive alcohol consumption and an unhealthy diet. In addition, individuals with genetic defects in apolipoprotein-CII (APOC2; an activator of lipoprotein lipase, which hydrolyses triglycerides to deliver fatty acids to body tissues) display hypertriglyceridemia even on a normal diet. Here, Yury Miller and colleagues generated mutant zebrafish bearing apoc2 loss-of-function mutations. These animals, fed a normal diet, exhibit severe hypertriglyceridemia and accumulate lipid and lipid-laden macrophages in the vasculature, which constitute early events in the development of human atherosclerotic lesions. Notably, injection of wild-type zebrafish plasma with functional Apoc2 or a human APOC2-mimetic peptide can rescue hypertriglyceridemia in the mutants. ...