miR-128 regulates differentiation of hair follicle mesenchymal stem cells into smooth muscle cells by targeting SMAD2

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• 作者：Zhihao Wang^a ; ^{wangzhih@jlu.edu.cn" class="auth_mail" title="E-mail the corresponding author} ; Li Pang^b ; Huiying Zhao^a ; Lei Song^c ; Yuehui Wang^a ; Qi Sun^d ; ^e ; Chunjie Guo^f ; Bin Wang^g ; Xiujiao Qin^a ; Aiqun Pan^d ; ^{panaq@jlu.edu.cn" class="auth_mail" title="E-mail the corresponding author}
• 关键词：3&prime ; -UTR ; 3&prime ; -untranslated region ; hHFMSC ; human hair follicle mesenchymal stem cell ; miR-128 ; microRNA-128 ; SMA ; smooth muscle actin ; SMC ; smooth muscle cell ; TGF-β1 ; transforming growth factor-β1
• 刊名：Acta Histochemica
• 出版年：2016
• 出版时间：May 2016
• 年：2016
• 卷：118
• 期：4
• 页码：393-400
• 全文大小：2043 K

文摘

Human hair follicle mesenchymal stem cells (hHFMSCs) are an important source of cardiovascular tissue engineering for their differentiation potential into smooth muscle cells (SMCs), yet the molecular pathways underlying such fate determination is unclear. MicroRNAs (miRNAs) are non-coding RNAs that play critical roles in cell differentiation. In present study, we found that miR-128 was remarkably decreased during the differentiation of hHFMSCs into SMCs induced by transforming growth factor-β1 (TGF-β1). Moreover, overexpression of miR-128 led to decreased expression of SMC cellular marker proteins, such as smooth muscle actin (SMA) and calponin, in TGF-β1-induced SMC differentiation. Further, we identified that miR-128 targeted the 3′-UTR of SMAD2 transcript for translational inhibition of SMAD2 protein, and knockdown of SMAD2 abrogated the promotional effect of antagomir-128 (miR-128 neutralizer) on SMC differentiation. These results suggest that miR-128 regulates the differentiation of hHFMSCs into SMCs via targeting SMAD2, a main transcription regulator in TGF-β signaling pathway involving SMC differentiation. The miR-128/SMAD2 axis could therefore be considered as a candidate target in tissue engineering and regenerative medicine for SMCs.