Overexpression of miR-200b inhibits the cell proliferation and promotes apoptosis of human hypertrophic scar fibroblasts in vitro
Overexpression of miR-200b inhibits the cell proliferation and promotes apoptosis of human hypertrophic scar fibroblasts in vitro
复制标题
DOI：
10.1111/1346-8138.12600
复制
发表时间：
2014-10-01
影响因子：
3.1
通讯作者：
Luo, Cheng-Qun
中科院分区：
文献类型：
--
作者：
Li, Ping;He, Quan-Yong;Luo, Cheng-Qun
增生性瘢痕导致畸形的外观和收缩的新生组织，导致患者的生理和心理问题。每年有数百万人遭受这些不适。新出现的证据已经报道了miRNA有助于增生性瘢痕形成或瘢痕疙瘩形成。在这项研究中，9个增生性瘢痕样本和匹配的正常皮肤组织被用来进行miRNA芯片。miRNA阵列结果显示miR-200 b在增生性瘢痕组织和人增生性瘢痕成纤维细胞中下调超过2倍，qPCR验证，提示miR-200 b与增生性瘢痕形成存在重要相关性。我们还发现miR-200 b通过影响人增生性瘢痕成纤维细胞I型和III型胶原合成、纤连蛋白表达和TGF-1/-SMA信号通路，调控细胞增殖和凋亡，从而影响增生性瘢痕的形成。因此，我们的研究提供了证据支持miR-200 b可能是肥大性瘢痕管理的有用靶点。
Hypertrophic scarring leads to a deformed appearance and contracted neogenetic tissue, resulting in physiological and psychological problems for patients. Millions of people suffer these discomforts each year. Emerging evidence has reported that miRNA contributed to hypertrophic scarring or keloid formation. In this study, nine hypertrophic scar samples and the matched normal skin tissues were used to perform a miRNA microarray. The results of miRNA array showed that miR-200b was downregulated by more than 2-fold, validated by qPCR in hypertrophic scar tissues and human hypertrophic scar fibroblasts, suggesting that there was an important correlation between miR-200b and hypertrophic scarring. We also found that miR-200b affected hypertrophic scarring through regulating the cell proliferation and apoptosis of human hypertrophic scar fibroblasts by affecting the collagen I and III synthesis, fibronectin expression and TGF-1/-SMA signaling. Thus, our study provides evidence to support that miR-200b may be a useful target for hypertrophic scarring management.