Inhibitor of DNA Binding 1 Is Induced during Kidney Ischemia-Reperfusion and Is Critical for the Induction of Hypoxia-Inducible Factor-1[alpha]

• Published in: BioMed research international 2016-01, Vol.2016
• Main Authors: Wen, Dan, Zou, Yan-Fang, Gao, Yao-Hui, Zhao, Qian, Xie, Yin-Yin, Shen, Ping-Yan, Xu, Yao-Wen, Xu, Jing, Chen, Yong-Xi, Feng, Xiao-Bei, Shi, Hao, Zhang, Wen
• Format: Article
• Language: English
• Subjects: Analysis; Apoptosis; Cancer; Cell cycle; Deoxyribonucleic acid; DNA; DNA-ligand interactions; Hypoxia; Immunohistochemistry; Ischemia; Kidneys; Medical research; Proteins; Regulation; RNA; Rodents; Transcription factors
• ISSN: 2314-6133; 2314-6141
• DOI: 10.1155/2016/4634386

In this study, rat models of acute kidney injury (AKI) induced by renal ischemia-reperfusion (I/R) and HK-2 cell models of hypoxia-reoxygenation (H/R) were established to investigate the expression of inhibitor of DNA binding 1 (ID1) in AKI, and the regulation relationship between ID1 and hypoxia-inducible factor 1 alpha (HIF-1α). Through western blot, quantitative real-time PCR, immunohistochemistry, and other experiment methods, the induction of ID1 after renal I/R in vivo was observed, which was expressed mainly in renal tubular epithelial cells (TECs). ID1 expression was upregulated in in vitro H/R models at both the protein and mRNA levels. Via RNAi, it was found that ID1 induction was inhibited with silencing of HIF-1α. Moreover, the suppression of ID1 mRNA expression could lead to decreased expression and transcription of HIF-1α during hypoxia and reoxygenation. In addition, it was demonstrated that both ID1 and HIF-1α can regulate the transcription of twist. This study demonstrated that ID1 is induced in renal TECs during I/R and can regulate the transcription and expression of HIF-1α.