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Background  Studies have suggested that estrogens may protect mice from AKI. Estrogen sulfotransferase ( SULT1E1 , or EST) plays an important role in estrogen homeostasis by sulfonating and deactivating estrogens, but studies on the role of  SULT1E1  in AKI are lacking.    Methods  We used the renal ischemia-reperfusion model to investigate the role of  SULT1E1  in AKI. We subjected wild-type mice,  Sult1e1  knockout mice, and  Sult1e1  knockout mice with liver-specific reconstitution of  SULT1E1  expression to bilateral renal ischemia-reperfusion or sham surgery, either in the absence or presence of gonadectomy. We assessed relevant biochemical, histologic, and gene expression markers of kidney injury. We also used wild-type mice treated with the  SULT1E1  inhibitor triclosan to determine the effect of pharmacologic inhibition of  SULT1E1  on AKI.    Results  AKI induced the expression of  Sult1e1  in a tissue-specific and sex-specific manner. It induced expression of  Sult1e1  in the liver in both male and female mice, but  Sult1e1  induction in the kidney occurred only in male mice. Genetic knockout or pharmacologic inhibition of  Sult1e1  protected mice of both sexes from AKI, independent of the presence of sex hormones. Instead, a gene profiling analysis indicated that the renoprotective effect was associated with increased vitamin D receptor signaling. Liver-specific transgenic reconstitution of  SULT1E1  in  Sult1e1  knockout mice abolished the protection in male mice but not in female mice, indicating that  Sult1e1 ’s effect on AKI was also tissue-specific and sex-specific.    Conclusions   SULT1E1  appears to have a novel function in the pathogenesis of AKI. Our findings suggest that inhibitors of  SULT1E1  might have therapeutic utility in the clinical management of AKI.

Inhibition of Estrogen Sulfotransferase (SULT1E1/EST) Ameliorates Ischemic Acute Kidney Injury in Mice