Stress-responsive gene TauT and acute kidney injury

Background. cisplatin is a commonly used chemotherapeutic agent that has a major limitation because of its nephrotoxicity. we have demonstrated that cisplatin down-regulates the expression of the taurine transporter gene (taut) in renal cells and that forced overexpression of taut protects against cisplatin-induced apoptosis in renal cells in vitro and in vivo. in the present study,we have investigated how taut is regulated by p53 and c-jun and its role during acute kidney injury (aki). methods. regulation of taut by p53 and c-jun was determined by reporter gene assay,dna binding,western blot analysis,and immunohistochemistry. results. taut was down-regulated by p53 and up-regulated by c-jun. two potential binding sites for c-jun were identified in the promoter region of taut. inhibition of c-jun n-terminal kinase (jnk) enhanced taut promoter activity. overexpression of taut protects against cisplatin-induced kidney injury in a taut transgenic mouse model. conclusions. our findings suggest that taut plays a critical role in renal function. expression of taut is negatively regulated by p53 and positively regulated by c-jun,which is mediated by the jnk signaling pathway. the outcome level of taut may determine the fate of renal cells during stress-induced aki. © 2010 han and chesney; licensee biomed central ltd.