TY - JOUR
T1 - Transforming growth factor-β2 inhibition of corneal endothelial proliferation mediated by prostaglandin
AU - Chen, Ko H.
AU - Hsu, Wen-Ming
AU - Chiang, Chien Cheng
AU - Li, Yen Shien
PY - 2003/6/1
Y1 - 2003/6/1
N2 - 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.
AB - 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.
KW - Aqueous humor
KW - Corneal endothelial cells
KW - Indomethacin
KW - Prostaglandin E2
KW - Transforming growth factor-β2
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U2 - 10.1076/ceyr.26.5.363.15442
DO - 10.1076/ceyr.26.5.363.15442
M3 - Article
C2 - 12868017
AN - SCOPUS:0042167360
VL - 26
SP - 363
EP - 370
JO - Current Eye Research
JF - Current Eye Research
SN - 0271-3683
IS - 6
ER -