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

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

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)363-370
Number of pages8
JournalCurrent Eye Research
Volume26
Issue number6
DOIs
Publication statusPublished - Jun 1 2003
Externally publishedYes

Fingerprint

Transforming Growth Factors
Dinoprostone
Prostaglandins
Indomethacin
Cell Proliferation
Corneal Endothelium
Immunoenzyme Techniques
Cultured Cells
Endothelial Cells
Cell Count

Keywords

  • Aqueous humor
  • Corneal endothelial cells
  • Indomethacin
  • Prostaglandin E2
  • Transforming growth factor-β2

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems

Cite this

Transforming growth factor-β2 inhibition of corneal endothelial proliferation mediated by prostaglandin. / Chen, Ko H.; Hsu, Wen-Ming; Chiang, Chien Cheng; Li, Yen Shien.

In: Current Eye Research, Vol. 26, No. 6, 01.06.2003, p. 363-370.

Research output: Contribution to journalArticle

Chen, Ko H. ; Hsu, Wen-Ming ; Chiang, Chien Cheng ; Li, Yen Shien. / Transforming growth factor-β2 inhibition of corneal endothelial proliferation mediated by prostaglandin. In: Current Eye Research. 2003 ; Vol. 26, No. 6. pp. 363-370.
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abstract = "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.",
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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

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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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