May 1997
Volume 38, Issue 6
Free
Articles  |   May 1997
Effects of dexamethasone on sodium-potassium-chloride cotransport in trabecular meshwork cells.
Author Affiliations
  • L K Putney
    Department of Human Physiology, University of California, Davis 95616-8644, USA.
  • J D Brandt
    Department of Human Physiology, University of California, Davis 95616-8644, USA.
  • M E O'Donnell
    Department of Human Physiology, University of California, Davis 95616-8644, USA.
Investigative Ophthalmology & Visual Science May 1997, Vol.38, 1229-1240. doi:
  • Views
  • PDF
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      L K Putney, J D Brandt, M E O'Donnell; Effects of dexamethasone on sodium-potassium-chloride cotransport in trabecular meshwork cells.. Invest. Ophthalmol. Vis. Sci. 1997;38(6):1229-1240.

      Download citation file:


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

      ×
  • Supplements
Abstract

PURPOSE: Previous studies in the authors' laboratory have shown that bovine and human trabecular meshwork (TM) cells possess a robust sodium-potassium-chloride (Na-K-Cl) cotransport system that functions in regulating intracellular volume and may play a central role in modulating outflow facility across the TM. Dexamethasone, which can induce ocular hypertension, has been found to increase resistance to aqueous outflow across the TM. The current study was conducted to investigate the hypothesis that alteration of TM cell Na-K-Cl cotransport function, regulation, or both may be an underlying factor in steroid-induced glaucoma. To this end, the authors evaluated the effects of dexamethasone treatment of TM cells on Na-K-Cl cotransport activity and cotransporter protein expression. METHODS: Cultured bovine and human TM cell monolayers were exposed to dexamethasone (10(-9) to 10(-6) M) for varying times, then evaluated for Na-K-Cl cotransport activity or harvested for cellular membrane proteins. Cotransport activity was assessed as bumetanide-sensitive K influx. Cotransport protein expression was evaluated by Western blot analysis of cellular proteins using a monoclonal antibody to the human colonic T84 epithelial cell Na-K-Cl cotransporter. RESULTS: The authors found that 24- and 48-hour exposures of human and bovine TM cells to dexamethasone stimulates Na-K-Cl cotransport activity (10(-8) to 10(-6) M dexamethasone in human cells; 10(-8) and 10(-7) M in bovine cells). The authors also found that dexamethasone (10(-8) M) stimulates Na-K-Cl cotransport activity of TM cells with exposure times as early as 12 hours and up to 5 days. In addition, the authors found that the level of Na-K-Cl cotransport protein expressed in TM cells is modulated by dexamethasone. When bovine or human TM cells are exposed to 10(-8) or 10(-6) M dexamethasone for 2 to 5 days, cotransporter protein expression is increased. With longer exposures, however, cotransporter protein levels decrease below control levels. Finally, the authors found that TM cells exposed to dexamethasone become unresponsive to regulation by hypertonicity and vasopressin. CONCLUSIONS: The authors' findings suggest that dexamethasone may be exerting its effect, at least in part, through altering Na-K-Cl cotransport function and regulation in TM cells.

×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×