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Urotensin II exerts antiapoptotic effect on NRK-52E cells through prostacyclin-mediated peroxisome proliferator-activated receptor alpha and Akt activation.

Hsu YH, Chen TH, Chen YC, Cheng CY, Sue YM, Chen JR, Chen CH.

Mol Cell Endocrinol. 2013 Dec 5;381(1-2):168-74.

Division of Nephrology, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.

Abstract

Urotensin II (UII) is a cyclic vasoactive peptide which is mainly expressed in kidneys. Although elevated plasma UII levels are associated with renal impairment, the influence of UII on renal injury is unclear. In this study, we monitored the influence of UII on gentamicin-induced apoptosis in rat tubular cells (NRK-52E). We found that UII significantly reduced gentamicin-induced apoptosis and apoptotic signals. Blocking endogenous UII secretion caused cells to be more susceptible to gentamicin. In gentamicin-treated mice, UII also expressed protective effect on renal tubular cells. UII was also found to induce prostacyclin (PGI2) production, which caused peroxisomal proliferator-activated receptor {Alpha} (PPAR{Alpha}) activation as revealed by both PGI2 synthase siRNA transfection and piroxicam treatment. Blockage of PPAR{Alpha} by siRNA transfection inhibited UII-induced Aktphosphorylation and the antiapoptotic effect of UII. Our results suggest that UII can protect renal tubular cells from gentamicin-induced apoptosis through PGI2-mediated PPAR{Alpha} and Akt activation.

Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.

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Urotensin II exerts antiapoptotic effect on NRK-52E cells through prostacyclin-mediated peroxisome proliferator-activated receptor alpha and Akt activation.