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Angiotensin II causes mesangial cell hypertrophy
P W Anderson1, Y S Do, W A Hsueh
1Department of Internal Medicine, Los Angeles County and University of Southern California Medical Center 90033.
Hypertension (Dallas, Tex. : 1979)
|January 1, 1993
Summary
Angiotensin II did not directly increase mesangial cell proliferation but stimulated protein synthesis. Losartan partially blocked these angiotensin II effects, suggesting its role in glomerulosclerosis.
Area of Science:
- Nephrology
- Cell Biology
- Molecular Biology
Background:
- Glomerulosclerosis is linked to mesangial cell growth.
- Angiotensin II is a vasoconstrictor and growth factor implicated in kidney disease.
Purpose of the Study:
- To investigate the direct impact of angiotensin II on cultured murine mesangial cell growth.
- To assess the role of angiotensin II in mesangial cell proliferation and protein synthesis.
Main Methods:
- Cultured adult murine mesangial cells were treated with angiotensin II (10(-6) M) for 48 hours.
- Cell growth was assessed by cell number, [3H]thymidine incorporation, [3H]leucine incorporation, and total protein content.
- The effect of losartan, an angiotensin II inhibitor, was evaluated.
Main Results:
- Angiotensin II did not significantly increase mesangial cell number or DNA synthesis ([3H]thymidine incorporation).
- Angiotensin II significantly increased protein synthesis ([3H]leucine incorporation) and total protein content.
- Losartan blocked a portion of the angiotensin II-induced protein synthesis and total protein increase.
Conclusions:
- Angiotensin II may not directly drive mesangial cell proliferation in vitro.
- Angiotensin II promotes mesangial cell protein synthesis, contributing to glomerulosclerosis.
- Inhibition of angiotensin II signaling with losartan partially mitigates these effects.