miR-483-5p 调控体外血管生成并靶向血清反应因子。
MiR-483-5p controls angiogenesis in vitro and targets serum response factor.
机构信息
Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China.
出版信息
FEBS Lett. 2011 Oct 3;585(19):3095-100. doi: 10.1016/j.febslet.2011.08.039. Epub 2011 Sep 1.
Angiogenesis, a key factor in ischemic heart disease, is rapidly initiated in response to hypoxic or ischemic conditions. MicroRNAs (miRNAs) are endogenously expressed small non-coding RNAs that regulate gene expression at post-transcriptional level. The recent discovery of the involvement of these RNAs in the control of angiogenesis renders them very attractive in the development of new approaches for restoring the angiogenic balance. In the present study, we explored that miR-483-5p, a microRNA embedded in the intron of insulin-like growth factor 2 (Igf2), acts as an endogenous angiogenesis-inhibiting factor. We identified that serum response factor (SRF) is one of miR-483-5p target genes. These findings indicated that the miR-483-5p-SRF pathway may offer a novel strategy for treatment with angiogenesis in ischemic heart disease patients.
血管生成是缺血性心脏病的一个关键因素,它会在缺氧或缺血的情况下迅速启动。microRNAs(miRNAs)是内源性表达的小非编码 RNA,可在转录后水平调节基因表达。最近发现这些 RNA 参与了血管生成的控制,这使得它们在开发新的方法来恢复血管生成平衡方面非常有吸引力。在本研究中,我们探讨了嵌入胰岛素样生长因子 2(Igf2)内含子中的 microRNA-483-5p 作为一种内源性血管生成抑制因子的作用。我们确定血清反应因子(SRF)是 miR-483-5p 的靶基因之一。这些发现表明,miR-483-5p-SRF 通路可能为缺血性心脏病患者的血管生成治疗提供一种新策略。