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Identification of apolipoprotein D as a cardioprotective gene using a mouse model of lethal atherosclerotic coronary artery disease Tsukamoto K; Mani DR; Shi J; Zhang S; Haagensen DE; Otsuka F; Guan J; Smith JD; Weng W; Liao R; Kolodgie FD; Virmani R; Krieger MProc Natl Acad Sci U S A 2013[Oct]; 110 (42): 17023-8Mice with homozygous null mutations in the HDL receptor (scavenger receptor class B, type I, or SR-BI) and apolipoprotein E (apoE) genes [SR-BI/apoE double KO (SR-BI(-/-)/apoE(-/-) or dKO) mice] spontaneously develop occlusive, atherosclerotic coronary artery disease (CAD) and die prematurely (50% mortality at 42 d of age). Using microarray mRNA expression profiling, we identified genes whose expression in the hearts of dKO mice changed substantially during disease progression [at 21 d of age (no CAD), 31 d of age (small myocardial infarctions), and 43 d of age (extensive myocardial infarctions) vs. CAD-free SR-BI(+/-)/apoE(-/-) controls]. Expression of most genes that increased >sixfold in dKO hearts at 43 d also increased after coronary artery ligation. We examined the influence and potential mechanism of action of apolipoprotein D (apoD) whose expression in dKO hearts increased 80-fold by 43 d. Analysis of ischemia/reperfusion-induced myocardial infarction in both apoD KO mice and wild-type mice with abnormally high plasma levels of apoD (adenovirus-mediated hepatic overexpression) established that apoD reduces myocardial infarction. There was a correlation of apoD's ability to protect primary cultured rat cardiomyocytes from hypoxia/reoxygenation injury with its potent ability to inhibit oxidation in a standard antioxidation assay in vitro. We conclude that dKO mice represent a useful mouse model of CAD and apoD may be part of an intrinsic cardioprotective system, possibly as a consequence of its antioxidation activity.|Animals[MESH]|Antioxidants/*metabolism[MESH]|Apolipoproteins D/*blood/genetics[MESH]|Apolipoproteins E/genetics/metabolism[MESH]|Cell Hypoxia/genetics[MESH]|Cells, Cultured[MESH]|Coronary Artery Disease/*blood/genetics/metabolism/pathology[MESH]|Disease Models, Animal[MESH]|Female[MESH]|Humans[MESH]|Mice[MESH]|Mice, Knockout[MESH]|Myocardial Infarction/blood/genetics/pathology[MESH]|Myocardial Reperfusion Injury/blood/genetics/pathology[MESH]|Myocardium/*metabolism/pathology[MESH]|Myocytes, Cardiac/*metabolism/pathology[MESH]|Rats, Wistar[MESH]|Scavenger Receptors, Class B/genetics/metabolism[MESH] |
