Down-regulation of miR-96 by bone morphogenetic protein signaling is critical for vascular smooth muscle cell phenotype modulation.
Down-regulation of miR-96 by bone morphogenetic protein signaling is critical for vascular smooth muscle cell phenotype modulation.
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DOI：
10.1002/jcb.24730
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发表时间：
2014-05
影响因子：
4
通讯作者：
Kang, Hara
中科院分区：
文献类型：
--
作者：
Kim, Sunghwan;Hata, Akiko;Kang, Hara
骨形态发生蛋白（BMP）信号通路是诱导和维持血管平滑肌细胞（VSMCs）收缩表型的关键。BMP信号传导的失活在血管发育异常和血管增殖性疾病中是常见的，如肺动脉高压。在此，我们确定microRNA-96（miR-96）作为VSMC表型的调节剂，响应于BMP 4信号传导。我们发现miR-96被BMP 4处理下调，这导致一种新的靶点Tribal样蛋白3（Trb 3）的去抑制。miR-96靶向位于Trb 3的3' UTR中的部分互补序列。Trb 3是BMP信号通路的重要正调控因子，并促进VSMC的收缩表型。总之，我们的研究证明了一种新的机制，通过抑制miR-96-Trb 3轴，通过BMP 4信号通路调节SMC特异性基因表达和诱导VSMC收缩表型。
The bone morphogenetic protein (BMP) signaling pathway is critical for the induction and maintenance of contractile phenotype in vascular smooth muscle cells (VSMCs). Inactivation of BMP signaling is common in abnormalities in vascular development and in vascular proliferative conditions, such as pulmonary artery hypertension. Herein, we identify microRNA-96 (miR-96) as a modulator of the VSMC phenotype in response to BMP4 signaling. We show that miR-96 is down-regulated by BMP4 treatment, which results in the derepression of a novel target, Tribbles-like protein 3 (Trb3). miR-96 targets a partially complementary sequence localized in the 3’ UTR of Trb3. Trb3 is an essential positive regulator of the BMP signaling pathway and promotes contractile phenotype in VSMCs. In conclusion, our study demonstrates a novel mechanism of regulation of SMC-specific gene expression and induction of a VSMC contractile phenotype by the BMP4 signaling pathway via suppression of the miR-96-Trb3 axis.
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