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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 induction in HK-2 cells H/R model. (a) Western blot analysis of ID1 in HK-2 cells under hypoxia (H) and reoxygenation (R). Cells for reoxygenation experienced 24 hours of hypoxia. β-actin served as the loading control. A representative blot from 3 independent experiments is shown. (b) Quantitative RT-PCR was used for analysis of ID1 mRNA levels in HK-2 cells under H/R. Data are expressed as mean ± SD for ID1 levels. β-actin mRNA served as the internal control (n = 3). ∗P < .05 compared with the prehypoxia controls. ID1, inhibitor of DNA binding 1; H/R, hypoxia-reoxygenation.
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fig4: ID1 induction in HK-2 cells H/R model. (a) Western blot analysis of ID1 in HK-2 cells under hypoxia (H) and reoxygenation (R). Cells for reoxygenation experienced 24 hours of hypoxia. β-actin served as the loading control. A representative blot from 3 independent experiments is shown. (b) Quantitative RT-PCR was used for analysis of ID1 mRNA levels in HK-2 cells under H/R. Data are expressed as mean ± SD for ID1 levels. β-actin mRNA served as the internal control (n = 3). ∗P < .05 compared with the prehypoxia controls. ID1, inhibitor of DNA binding 1; H/R, hypoxia-reoxygenation.

Mentions: After establishment of the H/R model in HK-2 cells, ID1 expression was assessed through western blot and qRT-PCR. The expression of ID1 was significantly increased during hypoxia and reduced following reoxygenation (Figure 4(a)). After 6 and 48 hours of reoxygenation, ID1 was upregulated again, although not remarkably. Moreover, the mRNA levels of ID1 were markedly elevated during hypoxia and reinduced after reoxygenation (Figure 4(b)).


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 induction in HK-2 cells H/R model. (a) Western blot analysis of ID1 in HK-2 cells under hypoxia (H) and reoxygenation (R). Cells for reoxygenation experienced 24 hours of hypoxia. β-actin served as the loading control. A representative blot from 3 independent experiments is shown. (b) Quantitative RT-PCR was used for analysis of ID1 mRNA levels in HK-2 cells under H/R. Data are expressed as mean ± SD for ID1 levels. β-actin mRNA served as the internal control (n = 3). ∗P < .05 compared with the prehypoxia controls. ID1, inhibitor of DNA binding 1; H/R, hypoxia-reoxygenation.
© Copyright Policy
Related In: Results  -  Collection

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

fig4: ID1 induction in HK-2 cells H/R model. (a) Western blot analysis of ID1 in HK-2 cells under hypoxia (H) and reoxygenation (R). Cells for reoxygenation experienced 24 hours of hypoxia. β-actin served as the loading control. A representative blot from 3 independent experiments is shown. (b) Quantitative RT-PCR was used for analysis of ID1 mRNA levels in HK-2 cells under H/R. Data are expressed as mean ± SD for ID1 levels. β-actin mRNA served as the internal control (n = 3). ∗P < .05 compared with the prehypoxia controls. ID1, inhibitor of DNA binding 1; H/R, hypoxia-reoxygenation.
Mentions: After establishment of the H/R model in HK-2 cells, ID1 expression was assessed through western blot and qRT-PCR. The expression of ID1 was significantly increased during hypoxia and reduced following reoxygenation (Figure 4(a)). After 6 and 48 hours of reoxygenation, ID1 was upregulated again, although not remarkably. Moreover, the mRNA levels of ID1 were markedly elevated during hypoxia and reinduced after reoxygenation (Figure 4(b)).

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