In vitro inhibition of proliferation, migration and epithelial-mesenchymal transition of human lens epithelial cells by fasudil
Autor: | Fu-Zhen Li, Wen-Wen Du, Shanshan Du, Fengyan Zhang, Ying Qi, Jingzhi Shao |
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Rok vydání: | 2018 |
Předmět: |
human lens epithelial cells
0301 basic medicine Myosin light-chain kinase Rho/Rock Cell epithelial-mesenchymal transition 02 engineering and technology 03 medical and health sciences lcsh:Ophthalmology TGF-β2 Medicine Epithelial–mesenchymal transition Protein kinase A IC50 business.industry Fasudil 021001 nanoscience & nanotechnology In vitro Cell biology Ophthalmology Basic Research 030104 developmental biology medicine.anatomical_structure lcsh:RE1-994 Phosphorylation 0210 nano-technology business fasudil |
Zdroj: | International Journal of Ophthalmology, Vol 11, Iss 8, Pp 1253-1257 (2018) |
ISSN: | 2227-4898 2222-3959 |
Popis: | Aim To study the potential role of fasudil as a treatment for posterior capsular opacification (PCO) of the human crystalline lens. Methods Human lens epithelial cells (HLECs; line SRA01/04) was exposed to transforming growth factor-β2 (TGF-β2) to induce the process of epithelial-mesenchymal transition (EMT). Fasudil was applied to the cell samples. Its effect on overall HLECs proliferation and migration was studied, as was its influence on EMT induction by TGF-β2 using cell migration assay, MTT colorimetric assay and Western blot assay. Results Fasudil inhibited the proliferation of SRA01/04. Its effect was time- and concentration-dependent. The migration of SRA01/04 cells was significantly reduced 24-72h after fasudil treatment, and the half maximal inhibitory concentration (IC50) was 22.37 µmol/mL at 72h. Reversal of the elongated, fibroblast-like shape changes induced by TGF-β2 in SRA01/04 cells was observed. Fasudil up-regulated the expression of Connexin43 protein and down-regulated the expression of α-SMA protein compared with the cells treated with TGF-β2. Furthermore, when exposed to fasudil, the phosphorylation of Rho-associated protein kinase (Rock) and myosin light chain (MLC) could not be activated in the cell preparations. Conclusion Fasudil suppresses the proliferation and migration of SRA01/04 cells, and inhibits the process of EMT induced by TGF-β2. These results suggest that fasudil may serve as a therapeutic agent for PCO. |
Databáze: | OpenAIRE |
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