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K. Chen, W. Hsu, C. Chiang, Y. Li; Transforming Growth Factor-b2 Inhibition of Corneal Endothelial Proliferation Mediated by Prostaglandin E2 . Invest. Ophthalmol. Vis. Sci. 2003;44(13):4737.
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Purpose: To investigate the role of prostaglandin (PG) E2 synthesis in mediating the inhibitory effect of transforming growth factor (TGF)-b2 on corneal endothelial (CE) proliferation. Methods: The PGE2 and cell proliferation assays were performed using cultured rabbit corneal endothelium. A PGE2-specific enzyme immunoassay was used to check PGE2 synthesis in supernatants of cells cultured with and without added TGF-b2 and/or indomethacin. To evaluate the inhibitory effects of PGE2 and TGF-b2 on CE proliferation, the number of cells grown with exogenous PGE2, or TGF-b2 with or without indomethacin pretreatment was determined. Results: TGF-b2, 0.5 to 50 ng/ml, increased the PGE2 secretion of CE dose-dependently in a time-dependent manner. Indomethacin (3 0.1 mg/ml) inhibited this PGE2 secretion to a low level (around 5-10 ng/ml) in the presence or absence of exogenous TGF-b2. Both exogenous TGF-b2 and PGE2 inhibited CE proliferation dose-dependently over a wide range of concentrations. Indomethacin reversed the inhibitory effects of TGF-b2 but not those of exogenous PGE2. In the medium supplemented with indomethacin, even in the presence of 50 ng/ml of TGF-b2, CE growth did not differ from control cultures. Conclusions: TGF-b2 stimulates PGE2 synthesis in CE and dose-dependently inhibits CE proliferation. Indomethacin extinguishes the inhibitory effects of TGF-b2 on CE proliferation but not the effect of exogenous PGE2. These data suggest that the antiproliferative effects of TGF-b2 on CE may be due to TGF-b2-induced synthesis of autocrine PGE2.
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