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Regulation of microRNA-302a in human and mouse macrophages after stimulation with modified low density lipoproteins. The main focus of the research is to explore whether microRNA-302a contributes to the maintenance of cholesterol homeostasis and therefore

Regulation of microRNA-302a in human and mouse macrophages after stimulation with modified low density lipoproteins. The main focus of the research is to explore whether microRNA-302a contributes to the maintenance of cholesterol homeostasis and therefore
修饰低密度脂蛋白刺激后人和小鼠巨噬细胞中 microRNA-302a 的调节。
批准号:
220300215
负责人:
Dr. Svenja Meiler
金额:
$0.0万
依托单位国家:
德国
项目类别:
Research Fellowships
财政年份:
2012
资助国家:
德国
项目状态:
已结题
起止时间:
2011-12-31 至 2014-12-31

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英文摘要
Cholesterol and other lipids play key roles in many physiological processes. Aberrant cholesterol/lipid homeostasis has been linked to a number of diseases including atherosclerosis. Therefore control of cholesterol levels is essential to human health. In addition to classical transcription regulators, a class of small endogenous double-stranded RNAs termed microRNAs (miRs) has emerged as important modulators of many cellular and physiological processes that affect organism growth, development, homeostasis, and disease. Recent studies have shown that specific miRs are regulated in modified low-density lipoprotein-treated macrophages, which can affect the cholesterol homeostasis in the cell. However involvement of miR-302a in lipid metabolism in macrophages has not been investigated so far. The aim of this study is to determine the potential role of miR-302a on the expression of genes involved in cellular cholesterol transport of mouse and human macrophages. To identify target genes of miR-302a and to manipulate miR-302a expression to regulate those genes in vitro assays will be used. To indicate the influence of miR-302a regarding cellular cholesterol transport and further more atherosclerosis in vivo experiments will be carried out. In this way miR-302a could be identified as an important therapeutic target for suppressing atherogenesis.
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