Purchase this article with an account.
R.R. Khankan, C. Spee, S. He, S.J. Ryan, D.R. Hinton; Upregulation of Fibronectin EDA in RPE Cells by Transforming Growth Factor Beta (TGF-b) . Invest. Ophthalmol. Vis. Sci. 2003;44(13):376.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Purpose: One of the earliest extracellular matrix (ECM) components expressed by RPE cells in response to injury is an alternatively spliced embryonic isoform of fibronectin, FN EDA. The purpose of this study was to determine the time and dose response effect of TGF-ß on FN EDA expression. Methods: Human fetal RPE cell cultures (passages 2-4) were exposed to increasing concentrations of both TGF-ß1 and TGF-ß2. FN EDA expression was analyzed at different time points in both cell supernatant and homogenates. Western blot and immunohistochemical analyses were performed utilizing a FN EDA-specific monoclonal antibody. Results: TGF-ß stimulation of RPE cells resulted in a marked dose-dependent increase in FN EDA that increased further with longer exposure to TGF-ß. Results were similar for both TGF-ßs. Conclusions: TGF-ß stimulates expression of FN EDA in RPE. Since TGF-ß is increased in a variety of ocular disorders, this result provides a mechanism by which TGF-ß may contribute to disease pathogenesis with an accumulation of ECM.
This PDF is available to Subscribers Only