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Vasoactive agents modulate matrix metalloproteinase-2 activity by mesangial cells
1Department of Medicine, Long Island Jewish Medical Center, New Hyde Park, New York 11040, USA.
The American Journal of the Medical Sciences
|December 1, 1995
Summary
Vasoactive agents like angiotensin II increase metalloproteinase activity (MA) in mesangial cells, potentially contributing to proteinuria. This effect is partly mediated by prostaglandin E2 and can be inhibited by amlodipine and prostaglandin inhibitors.
Area of Science:
- Nephrology
- Molecular Biology
- Pharmacology
Background:
- Vasoactive agents influence proteinuria by altering glomerular hemodynamics.
- The collagen component of the glomerular basement membrane is a potential target for vasoactive agents, influencing proteinuria.
- Mesangial cells play a role in regulating glomerular function and extracellular matrix degradation.
Purpose of the Study:
- To investigate the hypothesis that vasoactive agents alter metalloproteinase activity (MA) in mesangial cells.
- To determine the role of prostaglandin E2 in angiotensin II-induced MA.
- To evaluate the effects of amlodipine and prostaglandin inhibitors on MA.
Main Methods:
- Mesangial cells were treated with varying concentrations of angiotensin II.
- Metalloproteinase activity (MA) was measured using gelatin degradation assays.
- Cells were co-treated with angiotensin II and agents such as amlodipine, indomethacin, and meclofenamate.
Main Results:
- Angiotensin II significantly increased MA in mesangial cells in a dose-dependent manner.
- Amlodipine, a calcium channel blocker, inhibited both basal and angiotensin II-stimulated MA.
- Prostaglandin E2 increased MA, while prostaglandin inhibitors (indomethacin, meclofenamate) attenuated MA, including angiotensin II-induced activity.
Conclusions:
- Angiotensin II elevates MA in mesangial cells, suggesting a mechanism contributing to proteinuria.
- The increase in MA induced by angiotensin II appears to be partly mediated by prostaglandin E2 synthesis.
- Amlodipine and prostaglandin synthesis inhibitors demonstrate potential in modulating MA and may offer therapeutic benefits in proteinuric conditions.