September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Increased expression of glucocorticoid receptor B induces a novel transforming growth factor beta-2 isoform in trabecular meshwork cells
Author Affiliations & Notes
  • Adnan Dibas
    North Texas Eye Research Institute, Fort Worth, Texas, United States
  • Abbot F Clark
    North Texas Eye Research Institute, Fort Worth, Texas, United States
  • Thomas Yorio
    North Texas Eye Research Institute, Fort Worth, Texas, United States
  • Footnotes
    Commercial Relationships   Adnan Dibas, None; Abbot Clark, None; Thomas Yorio, None
  • Footnotes
    Support  EY016242
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 86. doi:
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      Adnan Dibas, Abbot F Clark, Thomas Yorio; Increased expression of glucocorticoid receptor B induces a novel transforming growth factor beta-2 isoform in trabecular meshwork cells. Invest. Ophthalmol. Vis. Sci. 2016;57(12):86.

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

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Abstract

Purpose : Glucocorticoids function via activation of the glucocorticoid receptor alpha (GRα), a mechanism that can be attenuated by an alternative spliced glucocorticoid receptor known as GR. Steroid use is linked to elevated intraocular pressure in ~30% of the human population. In addition, higher levels of TGFβ2 have been reported in the aqueous humor of glaucoma patients. In the current study, we investigated the effect of dexamethasone treatment on known glaucomatous markers in trabecular meshwork cells overexpressing GRα and GRβ.

Methods : Stably-transfected RFP-GRα and RFP-GRβ TM cell-lines were developed. Levels of plasminogen activator inhibitor-1 (PAI-1), lysyl oxidase (LOXL), collagen-I, collagen IV, and TGFβ2 in cells treated overnight with vehicle (ethanol) or dexamethasone (DEX) were studied using western blot in concentrated media.

Results : DEX treatment increased PAI-1, LOXL, pro-collagen-I, and collagen IV in TM5 and RFP-GRα-TM5 cells. However, DEX-induction of such proteins was inhibited in RFP-GRβ-TM5 cell-line. Overexpression of GRα and β receptors increased latent inactive TGFβ2 levels and a novel 30kDa isoform was detected in RFP-GRβ-TM5 cells only. DEX treatment inhibited the production of the active 13kDa TGFβ2 in all TM5 cell-lines.

Conclusions : Steroid treatment inhibited mature TGFβ2 production in TM cells. GRβ appears to exert novel actions in the trabecular meshwork independent of GRα.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.

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