Birc3 and Tip1 are upregulated in renal ischemia reperfusion injury

  • Gene. 2023 May 18;147492. doi: 10.1016/j.gene.2023.147492.
Sixu Wang  1 Meishan Zhao  1 Xiaofei Zhang  1 Ming Su  2 Ye Tian  3 Wei Qiu  4
Affiliations
  • 1. Department of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China.
  • 2. Department of Clinical Laboratory, Peking University People's Hospital, Beijing, People's Republic of China.
  • 3. Department of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China. Electronic address: [email protected].
  • 4. Department of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China. Electronic address: [email protected].
Abstract

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.

Keywords
Apoptosis; Birc3; Ischemia reperfusion injury; Renal transplantation; Tip1.
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