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.
- MeSH
- Epithelial Cells metabolism MeSH
- Cataract * metabolism MeSH
- TRPM Cation Channels * metabolism MeSH
- Humans MeSH
- Cell Proliferation MeSH
- Protein Serine-Threonine Kinases MeSH
- Signal Transduction MeSH
- Transforming Growth Factor beta2 metabolism pharmacology MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- MeSH
- Apoptosis genetics MeSH
- Research Support as Topic MeSH
- Insulin secretion MeSH
- Hydrogen Sulfide pharmacology metabolism MeSH
- Publication type
- Congress MeSH
