In vitro inhibition of proliferation, migration and epithelial-mesenchymal transition of human lens epithelial cells by fasudil

• Main Authors: Jing-Zhi Shao, Ying Qi, Shan-Shan Du, Wen-Wen Du, Fu-Zhen Li, Feng-Yan Zhang
• Format: Article
• Language: English
• Published: Press of International Journal of Ophthalmology (IJO PRESS) 2018-08-01
• Series: International Journal of Ophthalmology
• Subjects: 1257; fasudil; human lens epithelial cells; TGF-β2; Rho/Rock; epithelial-mesenchymal transition
• Online Access: http://www.ijo.cn/en_publish/2018/8/20180802.pdf

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.