Yang Shuai, Yao Haipei, Li Min, Li Hui, Wang Fang
Department of Ophthalmology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
PLoS One. 2016 Mar 28;11(3):e0152687. doi: 10.1371/journal.pone.0152687. eCollection 2016.
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.
研究长链非编码RNA（lncRNA）MALAT1在转化生长因子β1（TGF-β1）诱导的视网膜色素上皮（RPE）细胞上皮-间质转化（EMT）中的作用。
培养ARPE-19细胞并使其暴露于TGF-β1。通过形态学变化以及α-平滑肌肌动蛋白（αSMA）和纤连蛋白表达增加、E-钙黏蛋白和紧密连接蛋白1（ZO-1）在mRNA和蛋白质水平下调来确认APRE-19细胞的EMT。通过定量实时PCR检测RPE细胞中lncRNA MALAT1的表达。通过转染小干扰RNA（SiRNA）实现MALAT1的敲低。观察抑制MALAT1对EMT、迁移、增殖和TGFβ信号传导的影响。还在与增殖性玻璃体视网膜病变（PVR）玻璃体样本孵育的原代RPE细胞中检测MALAT1表达。
在与TGFβ1孵育的RPE细胞中，MALAT1的表达显著增加。MALAT1沉默至少部分通过激活Smad2/3信号传导来减弱TGFβ1诱导的RPE细胞的EMT、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TGFβ1诱导的人RPE细胞EMT，并为PVR的发病机制提供了新的认识。
