Kidney protection against ischemia/reperfusion injury by myofibrillogenesis regulator-1.

Abstract:

BACKGROUND/AIMS:Ischemia/reperfusion (I/R) injury is characterized by cytoskeletal reorganization and loss of polarity in proximal tubule epithelial cells. Previously, we showed that myofibrillogenesis regulator (MR)-1 promoted actin organization in cardiomyocytes. MR-1 is also expressed in the kidney. METHODS:In this study, we investigated MR-1 expression in acute renal failure induced by I/R in Sprague-Dawley rats. We determined the MR-1 expression and the ratio of fibrous actin (F-actin) to globular actin (G-actin). HK-2 cells were treated with or without hypoxia/reoxygenation (H/R), and MR-1 levels were increased by adenoviral overexpression or silenced by RNA interference. RESULTS:I/R and H/R resulted in cellular injury and decreases of MR-1, the F-/G-actin ratio, and myosin light chain (MLC)-2. MR-1 overexpression attenuated H/R-induced cell injury and loss of surface membrane polarity of actin. MR-1 overexpression also increased the expression and phosphorylation of MLC-2 and MLC kinase, which were decreased in MR-1-silenced and H/R-treated cells. CONCLUSION:Together, these data show that MR-1 promoted actin polarity on the membrane surface and protected HK-2 cells from H/R injury. The mechanism might involve the rapid organization of F-actin through the upregulation and phosphorylation of MLC-2.

journal_name

Am J Nephrol

authors

Wang X,Tao T,Ding R,Song D,Liu M,Xie Y,Liu X

doi

10.1159/000360141

subject

Has Abstract

pub_date

2014-01-01 00:00:00

pages

279-87

issue

4

eissn

0250-8095

issn

1421-9670

pii

000360141

journal_volume

39

pub_type

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