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

作者：Hsu Yung Ho; Chen Tso Hsiao; Chen Yen Cheng; Cheng Chung Yi; Sue Yuh Mou; Chen Jia Rung; Chen Cheng Hsien^*

来源：Molecular and Cellular Endocrinology, 2013, 381(1-2): 168-174.

DOI：10.1016/j.mce.2013.07.028

• Apoptosis
• Peroxisome proliferator-activated receptor alpha (PPAR alpha)
• Prostacyclin
• Akt
• Urotensin II

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 (PGI(2)) production, which caused peroxisomal proliferator-activated receptor alpha (PPAR alpha) activation as revealed by both PGI(2) synthase siRNA transfection and piroxicam treatment. Blockage of PPAR alpha by siRNA transfection inhibited UII-induced Akt phosphorylation and the antiapoptotic effect of UN. Our results suggest that UII can protect renal tubular cells from gentamicin-induced apoptosis through PGI(2)-mediated PPAR alpha and Akt activation.

• 出版日期2013-12-5