Long Non-Coding RNA MALAT1 Mediates Transforming Growth Factor Beta1-Induced Epithelial-Mesenchymal Transition of Retinal Pigment Epithelial Cells.
Long Non-Coding RNA MALAT1 Mediates Transforming Growth Factor Beta1-Induced Epithelial-Mesenchymal Transition of Retinal Pigment Epithelial Cells.
复制标题
长非编码 RNA MALAT1 介导转化生长因子 Beta1 诱导的视网膜色素上皮细胞上皮-间质转化
DOI：
10.1371/journal.pone.0152687
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发表时间：
2016
期刊：
影响因子：
3.7
通讯作者：
Wang F
中科院分区：
文献类型：
--
作者：
Yang S;Yao H;Li M;Li H;Wang F
目的：研究长非编码RNA MALAT1在转化生长因子β1(TGF1-β1)诱导的视网膜色素上皮细胞间充质转化中的作用。培养的ARPE-19细胞与转化生长因子-β-1共同作用，细胞形态发生改变，α-平滑肌肌动蛋白(α-SMA)和纤维连接蛋白表达增加，E-钙粘蛋白和透明带封闭蛋白-1(ZO-1)表达下调。实时定量聚合酶链式反应检测RPE细胞中LncRNA MALAT1的表达。通过导入小干扰RNA(SiRNA)实现MALAT1基因的敲除。观察抑制MALAT1对细胞内皮细胞转化、迁移、增殖和转化生长因子β信号的影响。在与增殖性玻璃体视网膜病变(PVR)玻璃体标本孵育的原代RPE细胞中也检测到MALAT1的表达。与转化生长因子β1共同孵育的RPE细胞中MALAT1的表达显著增加。MALAT1的沉默至少部分地通过激活Smad2/3信号通路来减弱转化生长因子β1诱导的RPE细胞的内胚层转移、迁移和增殖。在与PVR玻璃体样本孵育的原代RPE细胞中，MALAT1也显著增加。LncRNA MALAT1参与了转化生长因子β-1诱导的人视网膜色素上皮细胞上皮细胞转分化，为PVR的发病机制提供了新的认识。
To study the role of long non-coding RNA (lncRNA) MALAT1 in transforming growth factor beta 1 (TGF-β1)-induced epithelial-mesenchymal transition (EMT) of retinal pigment epithelial (RPE) cells. ARPE-19 cells were cultured and exposed to TGF-β1. The EMT of APRE-19 cells is confirmed by morphological change, as well as the increased expression of alpha-smooth muscle actin (αSMA) and fibronectin, and the down-regulation of E-cadherin and Zona occludin-1(ZO-1) at both mRNA and protein levels. The expression of lncRNA MALAT1 in RPE cells were detected by quantitative real-time PCR. Knockdown of MALAT1 was achieved by transfecting a small interfering RNA (SiRNA). The effect of inhibition of MALAT1 on EMT, migration, proliferation, and TGFβ signalings were observed. MALAT1 expression was also detected in primary RPE cells incubated with proliferative vitreoretinopathy (PVR) vitreous samples. The expression of MALAT1 is significantly increased in RPE cells incubated with TGFβ1. MALAT1 silencing attenuates TGFβ1-induced EMT, migration, and proliferation of RPE cells, at least partially through activating Smad2/3 signaling. MALAT1 is also significantly increased in primary RPE cells incubated with PVR vitreous samples. LncRNA MALAT1 is involved in TGFβ1-induced EMT of human RPE cells and provides new understandings for the pathogenesis of PVR.