August 1989
Volume 30, Issue 8
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Articles  |   August 1989
Dexamethasone induces specific proteins in human trabecular meshwork cells.
Author Affiliations
  • C A Partridge
    Department of Physiology, New York Medical College, Valhalla 10595.
  • B I Weinstein
    Department of Physiology, New York Medical College, Valhalla 10595.
  • A L Southren
    Department of Physiology, New York Medical College, Valhalla 10595.
  • M E Gerritsen
    Department of Physiology, New York Medical College, Valhalla 10595.
Investigative Ophthalmology & Visual Science August 1989, Vol.30, 1843-1847. doi:
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    • Get Citation

      C A Partridge, B I Weinstein, A L Southren, M E Gerritsen; Dexamethasone induces specific proteins in human trabecular meshwork cells.. Invest. Ophthalmol. Vis. Sci. 1989;30(8):1843-1847.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Previous studies have demonstrated the presence of high-affinity, glucocorticoid-specific receptors in explants of human outflow tissue and in cultured trabecular meshwork. Glucocorticoid-induced responses of scleral fibroblasts and trabecular meshwork cells were evaluated in this study. Incubation of human trabecular meshwork (HTM) and scleral fibroblast (HS) cells with 10(-7) M dexamethasone (DEX) results in a 60% inhibition of prostaglandin production. The effects of glucocorticoid treatment on cellular and secreted proteins using [35S] methionine incorporation were evaluated. Treatment of HTM cells cultured from two normal individuals with DEX induced the expression of [35S] methionine-labelled cellular proteins of 35, 65 and 70 kD, and secreted proteins of 40, 90 and 100 kD. Under the same experimental conditions, a 70 kD molecular weight cellular protein was induced in the HS cells. There were no apparent DEX-induced alterations in HS-secreted proteins. Since a functional common response to glucocorticoid treatment in both HS and HTM cells was inhibition of prostaglandin production, the dexamethasone-induced expression of the 70 kD protein in these cells may be related to this effect. Further studies are required to elucidate specific roles of the steroid-induced proteins in the effects of glucocorticoids on HTM and HS cells.

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