AI Article Synopsis

  • Steroid-induced glaucoma may arise from increased resistance to aqueous outflow due to an excess buildup of extracellular matrix components.
  • Research shows that corticosteroid treatment reduces the activity of certain enzymes (like stromelysin and tissue plasminogen activator) in both trabecular meshwork cell cultures and organ cultures.
  • The decrease in these proteolytic activities could lead to the accumulation of extracellular matrix components, potentially contributing to the development of steroid-induced glaucoma.

Article Abstract

Steroid-induced glaucoma is believed to result from increased aqueous outflow resistance and evidence suggests that this is the result of an excess accumulation of extracellular matrix components. This accumulation could result from an imbalance in the natural turnover of these components. We have investigated the effect of corticosteroid treatment of trabecular meshwork (TM) organ and cell cultures on the extracellular activities of the matrix metalloproteinases and plasminogen activators. We find that corticosteroid treatment results in decreased extracellular activity of stromelysin and tissue plasminogen activator in trabecular meshwork cell culture, and decreased 92 kDa collagenase IV, stromelysin, and tissue plasminogen activator in trabecular meshwork organ culture. These data suggest that decreased levels of proteolytic activities could account, in part, for the accumulation of some extracellular matrix components and be a contributing mechanism in steroid-induced glaucoma.

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Source
http://dx.doi.org/10.1006/exer.1993.1148DOI Listing

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