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Selenium's effects on MMP-2 and TIMP-1 secretion by human trabecular meshwork cells
Shannon M Conley1, Roberta L Bruhn, Parham V Morgan
1Department of Ophthalmology, University of Arizona, Tucson, Arizona 85711, USA. sconley@u.arizona.edu
Investigative Ophthalmology & Visual Science
|January 28, 2004
Summary
Selenium supplementation may increase glaucoma risk by altering extracellular matrix turnover in the eye. This study found selenium decreases MMP-2 and TIMP-1 in human trabecular meshwork cells, potentially raising intraocular pressure.
Area of Science:
- Ophthalmology
- Cell Biology
- Toxicology
Background:
- Glaucoma incidence is rising in individuals using selenium supplements.
- Human trabecular meshwork (HTM) cells maintain intraocular pressure homeostasis.
- Matrix metalloproteinases (MMPs) and their inhibitors (TIMPs) regulate extracellular matrix turnover.
Purpose of the Study:
- Investigate selenium's impact on HTM cell homeostasis.
- Determine selenium's effect on MMPs, TIMPs, and related signaling pathways in HTM cells.
Main Methods:
- HTM cell cultures treated with methyl seleninic acid (selenium compound).
- Analyzed MMP and TIMP secretion/activity using Western blot and zymography.
- Monitored extracellular-signal-related kinases 1 and 2 (ERK1/2) phosphorylation.
Main Results:
- Selenium decreased MMP-2 and TIMP-1 secretion dose-dependently.
- Selenium reduced ERK1/2 phosphorylation without altering total ERK levels.
- Observed dose-dependent, reversible changes in HTM cell-matrix interactions.
Conclusions:
- Selenium alters MMP-2/TIMP-1 balance, potentially disrupting extracellular matrix turnover.
- These changes may increase intraocular pressure, contributing to glaucoma development.
- Highlights a potential mechanism linking selenium supplements to increased glaucoma risk.