微小RNA-210-5p在真皮成纤维细胞分化过程中通过靶向信号转导和转录激活因子5A调控信号转导和转录激活因子3的激活。
MiR-210-5p regulates STAT3 activation by targeting STAT5A in the differentiation of dermal fibroblasts.
作者信息
Wei Shuyi, Qiu Ye
机构信息
Nanning Damai Microneedle Hair Technology Co., Ltd. Nanning Medical Aesthetic Clinic, Nanning 530021, Guangxi P.R. China.
Cancer Hospital Affiliated to Guangxi Medical University, Nanning 530021, Guangxi P.R. China.
出版信息
3 Biotech. 2021 May;11(5):243. doi: 10.1007/s13205-021-02777-w. Epub 2021 Apr 29.
Abstract
Elucidating the molecular mechanism of the microRNAs in skin fibrosis is critical for identifying a novel therapeutic strategy for hypertrophic scar (HS). In this study, it was shown that miR-210-5p is induced by TGFβ, and that overexpression of miR-210-5p promoted the differentiation of human dermal fibroblasts (HDFs) into myofibroblasts. STAT5A is required for TGFβ-induced STAT3 activity. Here, we show that miR-210-5p attenuated TGFβ-induced STAT3 signaling pathway by suppressing the expression of STAT5A. Taken together, the present study suggests that TGFβ-induced miR-210-5p reduced STAT5A expression, leading to aberrant activation of STAT3, and facilitate skin fibrosis in HDFs.
摘要
阐明微小RNA在皮肤纤维化中的分子机制对于确定肥厚性瘢痕（HS）的新型治疗策略至关重要。在本研究中，结果表明miR-210-5p由转化生长因子β（TGFβ）诱导，并且miR-210-5p的过表达促进人皮肤成纤维细胞（HDFs）向肌成纤维细胞分化。信号转导和转录激活因子5A（STAT5A）是TGFβ诱导的信号转导和转录激活因子3（STAT3）活性所必需的。在此，我们表明miR-210-5p通过抑制STAT5A的表达减弱了TGFβ诱导的STAT3信号通路。综上所述，本研究表明TGFβ诱导的miR-210-5p降低了STAT5A的表达，导致STAT3异常激活，并促进了HDFs中的皮肤纤维化。
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