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Related Experiment Videos

Dexamethasone induces specific proteins in human trabecular meshwork cells.

C A Partridge1, B I Weinstein, A L Southren

  • 1Department of Physiology, New York Medical College, Valhalla 10595.

Investigative Ophthalmology & Visual Science
|August 1, 1989
PubMed
Summary

Glucocorticoid treatment, like dexamethasone, inhibits prostaglandin production in human trabecular meshwork and scleral fibroblast cells. This treatment also induces specific protein expressions, potentially linked to the prostaglandin inhibition.

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Area of Science:

  • Ophthalmology
  • Cell Biology
  • Endocrinology

Background:

  • High-affinity glucocorticoid receptors are present in human outflow tissue and trabecular meshwork.
  • Glucocorticoids are known to influence cellular functions in the eye.

Purpose of the Study:

  • To evaluate glucocorticoid-induced responses in human scleral fibroblasts and trabecular meshwork cells.
  • To identify specific protein changes in response to dexamethasone treatment.

Main Methods:

  • Human trabecular meshwork (HTM) and scleral fibroblast (HS) cells were incubated with dexamethasone (DEX).
  • Prostaglandin production was measured.
  • [35S] methionine incorporation was used to evaluate cellular and secreted protein expression.

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Main Results:

  • Dexamethasone (10(-7) M) inhibited prostaglandin production by 60% in both HTM and HS cells.
  • DEX induced specific cellular proteins (35, 65, 70 kD) and secreted proteins (40, 90, 100 kD) in HTM cells.
  • A 70 kD cellular protein was induced in HS cells, with no significant changes in secreted proteins.

Conclusions:

  • Dexamethasone affects protein expression and prostaglandin production in ocular cells.
  • The induced 70 kD protein in both cell types may be related to the observed inhibition of prostaglandin production.
  • Further research is needed to understand the roles of these steroid-induced proteins.