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Regulation of cell-mediated collagen gel contraction in human retinal pigment epithelium cells by VEGF compared to TGF-{beta}2           ★★★
Regulation of cell-mediated collagen gel contraction in human retinal pigment epithelium cells by VEGF compared to TGF-{beta}2
作者:Tiepei Z… 文章来源:Eye Center, Second Affiliated Hospital, School of Medicine, Zhejiang University 点击数:240 更新时间:2011/9/13

Purpose: To explore the potential role of vascular endothelial growth factor (VEGF) compared to transforming growth factor (TGF)-beta2 in the regulation of human retinal pigment epithelium (RPE) cell-mediated collagen gel contraction.
Methods: TheRPE cell-mediated type I collagen gel contraction assay was performed to evaluate and compare the effect of VEGF and TGF-beta2. The number of viable RPE cells in the gel and the expression of alpha-smooth muscle actin (SMA) were analysed. Stimulated VEGF as well as TGF-beta2 secretion of RPE cells were also observed. Correlation analysis was performed to determine whether expression of alpha-SMA or the number of RPE cells was correlated with the contraction of the collagen gel.
Results: Both VEGF and TGF-beta2 caused a time-dependent gel contraction, associated with over-expression of alpha-SMA in RPE cells undergoing a fibroblast-like transformation. The decrease in volume of the collagen gel and increase in alpha-SMA expression were more significant in the TGF-beta2-treated group than in VEGF-treated group beginning at day 2, and the growth of RPE cells was significantly more inhibited in the TGF-beta2-treated group compared to the VEGF-treated group after day 1 (p < 0.05).  TGF-beta2 stimulation increased both VEGF mRNA expression and secretion. The alpha-SMA expression and the change in volume of collagen gel were significantly positively correlated in both experimental groups. There was no significant correlation between the number of RPE cells and the gel contraction.
Conclusions: Both VEGF and TGF-beta2 can cause induction of RPE cell-mediated collagen gel contraction in vitro via partial upregulation of alpha-SMA expression.

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