MiR-27b promotes sheep skeletal muscle satellite cell proliferation by targeting myostatin gene

文献类型： 外文期刊

第一作者： Zhang, Wei

作者： Zhang, Wei;Wang, Shi-Yin;Deng, Shuang-Yi;Gao, Li;Yang, Li-Wei;Liu, Xiao-Na;Shi, Guo-Qing;Zhang, Wei;Shi, Guo-Qing

作者机构：

关键词： miR-27b; myostatin gene; sheep; skeletal muscle; satellite cell

期刊名称：JOURNAL OF GENETICS （ 影响因子：1.166； 五年影响因子：1.212 ）

ISSN： 0022-1333

年卷期： 2018 年 97 卷 5 期

页码：

收录情况： SCI

摘要： To investigate the role of miR-27b in sheep skeletal muscle development, here we first cloned the sequence of sheep pre-miR-27b, then further investigated its expression pattern in sheep skeletal muscle in vivo, the relationship of miR-27b expression and sheep skeletal muscle satellite cell proliferation and differentiation in vitro, and then finally confirmed its target gene during this development process. MiR-27b sequence, especially its mature sequence, was conservative among different species. MiR-27b highly expressed in sheep skeletal muscle than other tissues. In skeletal muscle of Suffolk and Bashbay sheep, miR-27b was upregulated during foetal period and downregulated during postnatal period significantly (P<0.01), but it still kept a relatively higher expression level in skeletal muscle of postnatal Suffolk sheep than Bashbay. There is a potential target site of miR-27b on 3-UTR of sheep myostatin (MSTN) mRNA, and the double luciferase reporter assay proved that miR-27b could successfully bind on this site. When sheep satellite cells were in the proliferation status, miR-27b was upregulated and MSTN was downregulated significantly (P<0.01). When miR-27b mimics was transfected into sheep satellite cells, the cell proliferation was promoted and the protein level of MSTN was significantly downregulated (P<0.01). Moreover, miR-27b regulated its target gene MSTN by translation repression at an early step, and followed by inducing mRNA degradation in sheep satellite cells. Based on these results, we confirm that miR-27b could promote sheep skeletal muscle satellite cell proliferation by targeting MSTN and suppressing its expression.

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