Birc3 and Tip1 Are Upregulated in Renal Ischemia Reperfusion Injury

Identification of ischemia-reperfusion injury (I/R)-associated genes is essential for exploring I/R novel mechanisms. Previously, we screened differentially expressed genes in renal I/R mouse models and found that Tax1 binding protein 3 (Tip1) and baculoviral IAP repeat containing 3 (Birc3) are two upregulated genes in I/R. In the present study, we analyzed the expression of Tip1 and Birc3 in I/R models. We found that the expression of Tip1 and Birc3 was upregulated in I/R-treated mice, whereas Tip1 was downregulated and Birc3 was upregulated in oxygen-glucose deprivation/reoxygenation (OGD/R) in vitro models. By inhibiting Birc3 with AT-406 in I/R-treated mice, we observed that the serum creatinine or blood urea nitrogen did not vary. However, inhibition of Birc3 enhanced apoptosis of kidney tissues induced by I/R treatment. Consistently, we found that inhibition of Birc3 also increased the apoptosis rate in tubular epithelial cells induced by OGD/R. These data demonstrated that Tip1 and Birc3 were upregulated in I/R injury. The upregulation of Birc3 may protect against renal I/R injury.