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Related Experiment Videos

Defects in cortisol-metabolizing enzymes in primary open-angle glaucoma.

B I Weinstein, P Munnangi, G G Gordon

    Investigative Ophthalmology & Visual Science
    |June 1, 1985
    PubMed
    Summary

    Primary open-angle glaucoma (POAG) shows enzyme defects in trabecular meshwork cells, specifically increased delta 4-reductase and decreased 3-oxidoreductase. These enzymatic alterations may explain POAG

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    Area of Science:

    • Ophthalmology
    • Biochemistry
    • Cell Biology

    Background:

    • Primary open-angle glaucoma (POAG) is a leading cause of irreversible blindness.
    • Intraocular pressure elevation in POAG is linked to trabecular meshwork (TM) dysfunction.
    • Cortisol metabolism in the TM is not fully understood but may influence intraocular pressure.

    Purpose of the Study:

    • To investigate enzymatic defects in cortisol metabolism within human trabecular meshwork cells from POAG patients.
    • To determine if altered enzyme activity or quantity contributes to POAG pathogenesis.

    Main Methods:

    • Human trabecular meshwork cells were obtained from POAG and non-POAG donors.
    • Cortisol-metabolizing enzyme activities (delta 4-reductase and 3-oxidoreductase) were assayed in cell homogenates.

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  • Enzyme activities were compared between POAG and non-POAG groups under optimal conditions.

    • Main Results:

    • Trabecular meshwork cells from POAG patients exhibited a marked increase in delta 4-reductase activity.
    • A significant decrease in 3-oxidoreductase activity was observed in POAG trabecular meshwork cells.
    • Differences in enzyme activity were attributed to altered enzyme amounts, not cofactor or pH variations.

    Conclusions:

    • Human trabecular meshwork cells in POAG demonstrate specific enzymatic defects in cortisol metabolism.
    • These defects, particularly altered delta 4-reductase and 3-oxidoreductase levels, may underlie ocular hypertension in POAG.
    • The findings suggest a potential molecular basis for glucocorticoid sensitivity in POAG.