微小RNA-21通过Smad7促进瘢痕疙瘩中胶原蛋白的生成。
miR-21 promotes collagen production in keloid via Smad7.
作者信息
Zhou Renpeng, Wang Chen, Wen Congji, Wang Danru
机构信息
Department of Plastic and Reconstructive Surgery, Shanghai 9th People's Hospital, Shanghai Jiao Tong University School of Medicine, 639 Zhi Zao Ju Road, Shanghai 200011, PR China.
Department of Plastic Surgery, Yancheng First Peoples' Hospital, 16 Yue He Road, 224000, People's Republic of China.
出版信息
Burns. 2017 May;43(3):555-561. doi: 10.1016/j.burns.2016.09.013. Epub 2016 Oct 4.
OBJECTIVE
To explore the biological function of miR-21 in the formation of keloid.
METHODS
Normal skin and keloid tissue samples underwent histopathologic study and qPCR analysis. The expression of miR-21 and mRNA expression of Smad7, Col1A1, Col3A1 in fibroblasts derived from keloid tissue and normal skin tissue samples were detected by qPCR. Normal and keloid fibroblasts were transfected with miR-21 mimics or inhibitor respectively, and expression of Smad7, Col1A1 and Col3A1 were examined. After the normal fibroblasts were transfected with Smad7 siRNA, expression of Col1A1 and Col3A1 were detected by Western blot and qPCR analysis.
RESULTS
Collagen was obviously thick and disorganized in keloid tissue. The expression of miR-21, Col1A1 and Col3A1 in keloid tissue and keloid-derived fibroblasts were higher than that of normal counterparts, while the expression of Smad7 in keloid tissue and keloid-derived fibroblasts was lower. miR-21 mimics attenuated expression of Smad7, and enhanced the expression of Col1A1, Col3A1. Furthermore, the Smad7 siRNA increased expression of Col1A1and Col3A1.
CONCLUSIONS
miR-21 promoted collagen production in keloid by negatively regulating the expression of the Smad7.
目的
探讨微小RNA-21（miR-21）在瘢痕疙瘩形成中的生物学功能。
方法
对正常皮肤和瘢痕疙瘩组织样本进行组织病理学研究和定量聚合酶链反应（qPCR）分析。通过qPCR检测瘢痕疙瘩组织和正常皮肤组织样本来源的成纤维细胞中miR-21的表达以及Smad7、Ⅰ型胶原蛋白α1（Col1A1）、Ⅲ型胶原蛋白α1（Col3A1）的信使核糖核酸（mRNA）表达。分别用miR-21模拟物或抑制剂转染正常和成纤维细胞瘢痕疙瘩，检测Smad7、Col1A1和Col3A1的表达。用Smad7小干扰RNA（siRNA）转染正常成纤维细胞后，通过蛋白质免疫印迹法和qPCR分析检测Col1A1和Col3A1的表达。
结果
瘢痕疙瘩组织中胶原蛋白明显增厚且排列紊乱。瘢痕疙瘩组织和瘢痕疙瘩来源的成纤维细胞中miR-21、Col1A1和Col3A1的表达高于正常对照，而瘢痕疙瘩组织和瘢痕疙瘩来源的成纤维细胞中Smad7的表达较低。miR-21模拟物减弱了Smad7的表达，并增强了Col1A1、Col3A1的表达。此外，Smad7 siRNA增加了Col1A1和Col3A1的表达。
结论
miR-21通过负向调节Smad7的表达促进瘢痕疙瘩中胶原蛋白的产生。
Zotero 插件