Limits...
Inhibitor of DNA Binding 1 Is Induced during Kidney Ischemia-Reperfusion and Is Critical for the Induction of Hypoxia-Inducible Factor-1α.

Wen D, Zou YF, Gao YH, Zhao Q, Xie YY, Shen PY, Xu YW, Xu J, Chen YX, Feng XB, Shi H, Zhang W - Biomed Res Int (2016)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Department of Nephrology, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200025, China.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus

ID1 and HIF-1α protein induction in the rat I/R injury model. (a, b) Western blot analysis of ID1 and HIF-1α expression in the kidney cortex after I/R. The expression of β-actin was examined as the loading control. A representative blot from 3 independent experiments is shown. (c, d) The histogram shows the average volume densities corrected for β-actin (n = 3). ∗P < .05 compared with the preischemia controls. ID1, inhibitor of DNA binding 1; HIF-1α, hypoxia-inducible factor-1 alpha; I/R, ischemia-reperfusion.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4835634&req=5

fig1: ID1 and HIF-1α protein induction in the rat I/R injury model. (a, b) Western blot analysis of ID1 and HIF-1α expression in the kidney cortex after I/R. The expression of β-actin was examined as the loading control. A representative blot from 3 independent experiments is shown. (c, d) The histogram shows the average volume densities corrected for β-actin (n = 3). ∗P < .05 compared with the preischemia controls. ID1, inhibitor of DNA binding 1; HIF-1α, hypoxia-inducible factor-1 alpha; I/R, ischemia-reperfusion.

Mentions: To investigate ID1 and HIF-1α expression in vivo, the I/R model in Sprague-Dawley rats was established as described previously [10]. Western blot analysis of kidney cortex showed the induction of ID1 and HIF-1α expression during reperfusion in vivo. ID1 expression was elevated immediately and transiently after reperfusion for 2 hours, and a reinduction was observed after reperfusion for 12 hours (Figure 1(a)). After statistical analysis of the grey level, ID1 was determined to be induced significantly after reperfusion for 2, 12, and 24 hours, and it was markedly reduced after 48 and 72 hours of reperfusion (Figure 1(c)). HIF-1α protein was elevated after reperfusion for 2 hours (Figure 1(b)), and the analysis of the grey level showed significant upregulation of it (Figure 1(d)).


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

Wen D, Zou YF, Gao YH, Zhao Q, Xie YY, Shen PY, Xu YW, Xu J, Chen YX, Feng XB, Shi H, Zhang W - Biomed Res Int (2016)

ID1 and HIF-1α protein induction in the rat I/R injury model. (a, b) Western blot analysis of ID1 and HIF-1α expression in the kidney cortex after I/R. The expression of β-actin was examined as the loading control. A representative blot from 3 independent experiments is shown. (c, d) The histogram shows the average volume densities corrected for β-actin (n = 3). ∗P < .05 compared with the preischemia controls. ID1, inhibitor of DNA binding 1; HIF-1α, hypoxia-inducible factor-1 alpha; I/R, ischemia-reperfusion.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4835634&req=5

fig1: ID1 and HIF-1α protein induction in the rat I/R injury model. (a, b) Western blot analysis of ID1 and HIF-1α expression in the kidney cortex after I/R. The expression of β-actin was examined as the loading control. A representative blot from 3 independent experiments is shown. (c, d) The histogram shows the average volume densities corrected for β-actin (n = 3). ∗P < .05 compared with the preischemia controls. ID1, inhibitor of DNA binding 1; HIF-1α, hypoxia-inducible factor-1 alpha; I/R, ischemia-reperfusion.
Mentions: To investigate ID1 and HIF-1α expression in vivo, the I/R model in Sprague-Dawley rats was established as described previously [10]. Western blot analysis of kidney cortex showed the induction of ID1 and HIF-1α expression during reperfusion in vivo. ID1 expression was elevated immediately and transiently after reperfusion for 2 hours, and a reinduction was observed after reperfusion for 12 hours (Figure 1(a)). After statistical analysis of the grey level, ID1 was determined to be induced significantly after reperfusion for 2, 12, and 24 hours, and it was markedly reduced after 48 and 72 hours of reperfusion (Figure 1(c)). HIF-1α protein was elevated after reperfusion for 2 hours (Figure 1(b)), and the analysis of the grey level showed significant upregulation of it (Figure 1(d)).

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Department of Nephrology, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200025, China.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus