Proteasome inhibition by chronic oxidative stress in human trabecular meshwork cells

Proteasome inhibition by chronic oxidative stress in human trabecular meshwork cells The pathophysiologic mechanisms leading to the malfunction of the trabecular meshwork (TM)–Schlemm’s canal (SC) outflow pathway in glaucoma are still unclear. We hypothesize that chronic oxidative stress may contribute to the malfunction of the outflow pathway by impairing the intracellular proteasome system of the cells, decreasing the ability of the tissue to modulate outflow resistance. To study the effects of chronic oxidative stress on proteasome function, primary cultures of human TM cells were incubated under 40% oxygen and proteasome activity was analyzed by measuring the accumulation of enhanced green fluorescent protein fused to a PEST motif. Changes in proteasome content, cellular senescence, and cell viability were also monitored. After 10 days of exposure to chronic oxidative stress, TM cells showed a marked decline in proteasome activity that was associated with premature senescence and decreased cell viability. These results suggest that proteasome failure may be involved in glaucoma pathophysiology. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Biochemical and Biophysical Research Communications Elsevier

Proteasome inhibition by chronic oxidative stress in human trabecular meshwork cells

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Publisher
Elsevier
Copyright
Copyright © 2003 Elsevier Inc.
ISSN
0006-291x
D.O.I.
10.1016/S0006-291X(03)01385-8
Publisher site
See Article on Publisher Site

Abstract

The pathophysiologic mechanisms leading to the malfunction of the trabecular meshwork (TM)–Schlemm’s canal (SC) outflow pathway in glaucoma are still unclear. We hypothesize that chronic oxidative stress may contribute to the malfunction of the outflow pathway by impairing the intracellular proteasome system of the cells, decreasing the ability of the tissue to modulate outflow resistance. To study the effects of chronic oxidative stress on proteasome function, primary cultures of human TM cells were incubated under 40% oxygen and proteasome activity was analyzed by measuring the accumulation of enhanced green fluorescent protein fused to a PEST motif. Changes in proteasome content, cellular senescence, and cell viability were also monitored. After 10 days of exposure to chronic oxidative stress, TM cells showed a marked decline in proteasome activity that was associated with premature senescence and decreased cell viability. These results suggest that proteasome failure may be involved in glaucoma pathophysiology.

Journal

Biochemical and Biophysical Research CommunicationsElsevier

Published: Aug 22, 2003

References

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