Korean J Nephrol.
2006 Sep;25(5):705-715.
Angiotensin II Effect on alpha-Actinin in Glomerular Epithelial Cells
- Affiliations
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- 1Department of Internal Medicine, College of Medicine, Chungbuk National University Cheongju, Korea.
- 2Department of Pediatrics, College of Medicine, Chungbuk National University Cheongju, Korea. tsha@chungbuk.ac.kr
Abstract
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BACKGROUND: Angiotensin II plays a potential role in renal injury not only by its vasoconstrictive effects but also its biochemical effects. alpha-Actinin, an actin-linked glycoprotein, is expressed in podocytes and known to be rearranged and changed in various glomerular diseases. We investigated the effect of angiotensin II on the alpha-actinin in the glomerular epithelial cells to find out the fact that it could be prevented by losartan, a type 1 angiotensin receptor antagonist.
METHODS
Glomerular epithelial cells were treated with various concentrations of angiotensin II in culture media, and then we compared the localization and amount of alpha-actinin by confocal microscopy and Western blot analysis, respectively. We also compared the differences in the localization and protein amount of alpha-actinin by various concentrations of losartan in the presence of angiotensin II. In addition, we tried to observe the mRNA expression of alpha-actinin via RT-PCR.
RESULTS
The fluorescent and band intensities of alpha-actinin were decreased by angiotensin II in a dose-dependent manner by confocal microscopy and Western blot analysis, respectively. These changes of alpha-actinin by angiotensin II were reversed by losartan in dose dependent manner. Angiotensin II also changed the distribution of alpha-actinin from peripheral to inner cytoplasm in dose-dependent manner, which was also reversed by losartan. The different expression of alpha-actinin m-RNA by RT-PCR were unremarkable.
CONCLUSIONS
Angiotensin II decreases the amount of alpha-actinin protein and and makes cytoskeletal changes in glomerular epithelial cells, which could be reversed by losartan. It suggests that it could be prevented by angiotensin II AT1 receptor blockers.