Transforming growth factor-β2 inhibition of corneal endothelial proliferation mediated by prostaglandin

Ko H. Chen, Wen-Ming Hsu, Chien Cheng Chiang, Yen Shien Li

研究成果: 雜誌貢獻文章同行評審

20 引文 斯高帕斯(Scopus)

摘要

Purpose. To determine the influence of Prostaglandin (PG) E2 on transforming growth factor (TGF)-β2-mediated inhibitory effects on the proliferation of corneal endothelial cells (CE). 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-β2 and/or indomethacin. To evaluate the inhibitory effects of PGE2 and TGF-β2 on CE proliferation, the number of cells grown with exogenous PGE2, or TGF-β2 with or without indomethacin pretreatment was determined. Results. TGF-β2, 0.5 to 50 ng/ml, increased the PGE2 secretion of CE dose-dependently in a time-dependent manner. Indomethacin (≥0.1 μg/ml) inhibited this PGE2 secretion to a low level (around 5-10 ng/ml) in the presence or absence of exogenous TGF-β2. Both exogenous TGF-β2 and PGE2 inhibited CE proliferation dose-dependently over a wide range of concentrations. Indomethacin reversed the inhibitory effects of TGF-β2 but not those of exogenous PGE2. In the medium supplemented with indomethacin, even in the presence of 50 ng/ml of TGF-β2, CE growth did not differ from control cultures. Conclusions. TGF-β2 stimulates PGE2 synthesis in CE and inhibits CE proliferation in a dose-dependent manner. Indomethacin extinguishes the inhibitory effects of TGF-β2 on CE proliferation but not the effect of exogenous PGE2. These data suggest that the antiproliferative effects of TGF-β2 on CE may be possibly due to TGF-β2-induced synthesis of PG, most likely PGE2.

原文英語
頁(從 - 到)363-370
頁數8
期刊Current Eye Research
26
發行號6
DOIs
出版狀態已發佈 - 六月 1 2003
對外發佈

ASJC Scopus subject areas

  • 眼科
  • 感覺系統

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