Transforming growth factor-beta1 induces alpha-smooth muscle actin expression and fibronectin synthesis in cultured human retinal pigment epithelial cells.

Abstract

Proliferative vitreoretinopathy is a serious complication of retinal detachment, yet its pathogenesis is not fully understood. Retinal pigment epithelial cells and glial cells are found in the fibrous membranes in proliferative vitreoretinopathy. Many cytokines are involved in the pathology. Transforming growth factor (TGF)-beta, a cytokine found in serum, has been shown to be an important factor regulating the synthesis of fibrous extracellular matrix in proliferative vitreoretinopathy. Cultured human retinal pigment epithelial cells were used in the experiments. The effects of TGF-beta1 on phenotype and function in retinal pigment epithelial cells were recorded as changes in the expression of alpha-smooth muscle actin and fibronectin synthesis using immunohistochemistry and enzyme-linked immunosorbent assay, respectively. TGF-beta1 induced the expression of alpha-smooth muscle actin (P < 0.0001, n = 3), and significantly increased the synthesis of fibronectin by cultured human retinal pigment epithelial cells (P < 0.01, n = 4). Elevated levels of TGF-beta1 in proliferative vitreoretinopathy may contribute to phenotype changes in retinal pigment epithelial cells leading to matrix deposition and contraction. Since the elevated levels of TGF-beta1 may emanate from a number of diverse sources in proliferative vitreoretinopathy, developing an antagonist to TGF-beta1 may offer an approach to the treatment of proliferative vitreoretinopathy.