Birc3 and Tip1 are upregulated in renal ischemia reperfusion injury
•Birc3 and Tip1 were upregulated in renal ischemia reperfusion (I/R) mice model.•Birc3 was upregulated in human tubular epithelial cells after I/R, while Tip1 was downregulated.•Birc3 may play a protective role in I/R by resisting apoptosis of renal tubular epithelial cells. Identification of ischem...
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Published in: | Gene Vol. 876; p. 147492 |
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Main Authors: | , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Netherlands
Elsevier B.V
05-08-2023
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Subjects: | |
Online Access: | Get full text |
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Summary: | •Birc3 and Tip1 were upregulated in renal ischemia reperfusion (I/R) mice model.•Birc3 was upregulated in human tubular epithelial cells after I/R, while Tip1 was downregulated.•Birc3 may play a protective role in I/R by resisting apoptosis of renal tubular epithelial cells.
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. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0378-1119 1879-0038 |
DOI: | 10.1016/j.gene.2023.147492 |