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Role of connective transforming growth factor in the development of posterior capsule opacification in bovine lens epithelial cells         ★★★
Role of connective transforming growth factor in the development of posterior capsule opacification in bovine lens epithelial cells
作者:陈博 文章来源:武汉同济医院 点击数:595 更新时间:2012/9/13 11:58:00
SummaryPosterior capsule opacification (PCO), the major complication of cataract surgery, wouldinduce visual loss. In this study,the involvement of connective transforming growth factor (CTGF) in the development of posterior capsule opacification (PCO) in bovine lens epithelial cells (BLECs) has been investigated.Perparing by recombination CTGF, the migration ability of BLECs was mesured by transwell inserts assay. After treating with recombination trasforming growth factor-beta1(TGF-beta1), in combination with CTGF short interference RNA (SiRNA) in BLECs, gene and protein expression ofα-smooth muscle actin (alpha-SMA), fibronectin (FN) and CTGF were characterized with Real-Timereverse transcriptase-polymerase chain reaction (Real-Time RT-PCR) and Western blot. In addition, JNK and PI3K/Akt were evaluated by Western blot for elucidating the mechanism of CTGF-induced FN production.As the downstream regulatory factor of TGF-beta, CTGF could significant promote bovine lens epithelial cells migration. The expression of CTGF was blocked by CTGF SiRNA in BLECs, and the expression ofalpha-SMA and FN also decreasedat mRNA and protein level. In the presence of JNK inhibitor (SP-600125) or transfected by JNK SiRNA, CTGF-induced protein expression of FN increase was completely inhibited. Akt inhibitor (LY-294002) and Akt SiRNA had no effect on CTGF-stimulated protein expression of FN.These results suggest that CTGF play an important role in thelens epithelial cells migration, transdifferentiation and deposition ofextracellular materials(ECM) in posterior capsule opacification. FN expression which induced by CTGF is mediated through the JNK pathway, but not affected by PI3K/Akt pathway. Therefore, RNA interference inhibits the expression of CTGF would be anew molecular target in prevention and therapeutics of PCO.
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