TRPM7 Elicits Proliferation and Differentiation of Human Lens Epithelial Cells through the TGF-β/Smad Pathways.

IF 0.8 4区 生物学 Q4 BIOLOGY
G Yang, Y Wu, S Tang
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引用次数: 0

Abstract

Epithelial-mesenchymal transition (EMT) plays a crucial role in the development of cataract. This study aimed to explore the effects of TRPM7 on the proliferation and differentiation of human lens epithelial cells. TRPM7 was over-expressed in LECs treated with TGF-β2. Down-regulation of TRPM7 attenuated the increase in cell viability and cell proliferation induced by TGF-β2. The LEC migration induced by TGF-β2 was also repressed by down-regulation of TRPM7. Epithelial-specific protein E-cadherin was up-regulated through knock-down of TRPM7. EMT-specific proteins, α-SMA, fibronectin and vimentin, were down-regulated through knockdown of TRPM7. Moreover, phosphorylation of Smad2 and Smad3 was also prevented by inhibition of TRPM7. Therefore, TRPM7 elicited LEC proliferation and EMT through enhancing activation of the TGF-β/Smad pathways, implying a new therapeutic target for cataract.

TRPM7通过TGF-β/Smad通路诱导人晶状体上皮细胞增殖和分化
上皮-间质转化(Epithelial-mesenchymal transition, EMT)在白内障的发生发展中起着至关重要的作用。本研究旨在探讨TRPM7对人晶状体上皮细胞增殖和分化的影响。TGF-β2处理的LECs中TRPM7过表达。下调TRPM7可减弱TGF-β2诱导的细胞活力和细胞增殖的增加。下调TRPM7也可抑制TGF-β2诱导的LEC迁移。上皮特异性蛋白E-cadherin通过敲除TRPM7而上调。emt特异性蛋白α-SMA、纤维连接蛋白和vimentin通过敲低TRPM7而下调。此外,抑制TRPM7也能阻止Smad2和Smad3的磷酸化。因此,TRPM7通过增强TGF-β/Smad通路的激活,诱导LEC增殖和EMT,可能是白内障新的治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Folia Biologica-Krakow
Folia Biologica-Krakow 医学-生物学
CiteScore
1.10
自引率
14.30%
发文量
15
审稿时长
>12 weeks
期刊介绍: Folia Biologica (Kraków) is an international online open access journal accepting original scientific articles on various aspects of zoology: phylogeny, genetics, chromosomal studies, ecology, biogeography, experimental zoology and ultrastructural studies. The language of publication is English, articles are assembled in four issues per year.
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