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B 细胞易位基因是 miR-142-5p 的直接靶标,通过下调细胞周期进程抑制血管平滑肌细胞增殖。

B cell translocation gene, a direct target of miR-142-5p, inhibits vascular smooth muscle cell proliferation by down-regulating cell cycle progression.

机构信息

Heart Research Center of Chonnam National University Hospital, Gwangju 501-757, Republic of Korea.

出版信息

FEBS Lett. 2013 Aug 2;587(15):2385-92. doi: 10.1016/j.febslet.2013.06.005. Epub 2013 Jun 13.

DOI:10.1016/j.febslet.2013.06.005
PMID:23770100
Abstract

Vascular smooth muscle cell (VSMC) proliferation plays a key role in neointimal hyperplasia and restenosis. Here we report the role of the microRNA miR-142-5p and its downstream target genes on the proliferation of cultured VSMCs. miR-142-5p promoted VSMC proliferation by down-regulating B cell translocation gene 3 (BTG3). We found that BTG3 inhibited the expression of cell cycle regulatory genes and cell growth. As shown by luciferase reporter assay, miR-142-5p bound directly to the 3'-untranslated region of BTG3. Overexpression of miR-142-5p induced expression of cell cycle regulatory genes. Thus, BTG3, a novel, direct target of miR-142-5p, negatively regulates VSMC proliferation.

摘要

血管平滑肌细胞(VSMC)增殖在新生内膜增生和再狭窄中起着关键作用。在这里,我们报告了 microRNA miR-142-5p 及其下游靶基因在培养的 VSMC 增殖中的作用。miR-142-5p 通过下调 B 细胞易位基因 3(BTG3)促进 VSMC 增殖。我们发现 BTG3 抑制细胞周期调控基因和细胞生长的表达。正如荧光素酶报告基因实验所示,miR-142-5p 直接结合到 BTG3 的 3'-非翻译区。miR-142-5p 的过表达诱导细胞周期调控基因的表达。因此,BTG3 是 miR-142-5p 的一个新的直接靶基因,负调控 VSMC 的增殖。

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