國家衛生研究院 NHRI:Item 3990099045/9335
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    題名: MicroRNA-451 protects against atherosclerotic plaque formation by directly targeting ras-associated protein 5a in vascular smooth muscle cells
    作者: Chen, LJ;Chuang, L;Huang, YH;Chien, S;Chiu, JJ
    貢獻者: Institute of Cellular and Systems Medicine
    摘要: MicroRNA-451 (miR-451) modulates erythroid differentiation and human malignancy. However, its role in the regulation of vascular smooth muscle cell (VSMC) function in health and disease remains unclear. Using a combination of in vitro system and in vivo investigations on experimental animals and human clinical specimens to clarify the function of miR-451 in VSMCs. In situ hybridization showed that miR-451 was significantly expressed in VSMCs of the medial layer in diseased human coronary arteries. In vitro study, culturing VSMCs on fibrillar collagen increased miR-451 level and led to low proliferative and anti-inflammatory responses; these effects were diminished by anti-miR-451. We identified that Rab5a was targeted by miR-451 to modulate VSMC proliferation and inflammation. In rat studies, overexpression of miR-451 and lentivirus-mediated Rab5a silencing markedly suppressed the neointima formation induced by balloon injury. The level of circulating miR-451 of blood plasma in patients with coronary artery disease and apolipoprotein E knockout mice (ApoE-/-) fed with a high-cholesterol diet was significantly lower than control group. Increase of circulating miR-451 by tail vein injection with agomir-451 in ApoE-/- mice fed with a high-cholesterol diet for three months decreased atherosclerotic lesion formation. Our findings indicate that miR-451, by targeting Rab5a, inhibits VSMC proliferation and inflammation in cultured VSMCs in vitro and suppresses neointima formation in injured arteries in vivo.
    日期: 2015-04
    關聯: FASEB Journal. 2015 Apr;29(1, Suppl.):Abstract number 1047.2.
    Link to: http://www.fasebj.org/content/29/1_Supplement/1047.2
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0892-6638&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000361722708093
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