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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

Location of ID1 and HIF-1α expression in I/R-injured rat kidney tissue. Immunohistochemical staining for ID1 and HIF-1α in the kidney tissue of I/R and sham-operated rats. (a) Increased staining for ID1 in renal TECs after 2, 6, 12, and 24 hours of reperfusion. (b) Increased staining for HIF-1α in renal TECs after 2 hours of reperfusion. Original magnification, ×200. ID1, inhibitor of DNA binding 1; HIF-1α, hypoxia-inducible factor-1 alpha; I/R, ischemia-reperfusion; TECs, tubular epithelial cells.
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fig2: Location of ID1 and HIF-1α expression in I/R-injured rat kidney tissue. Immunohistochemical staining for ID1 and HIF-1α in the kidney tissue of I/R and sham-operated rats. (a) Increased staining for ID1 in renal TECs after 2, 6, 12, and 24 hours of reperfusion. (b) Increased staining for HIF-1α in renal TECs after 2 hours of reperfusion. Original magnification, ×200. ID1, inhibitor of DNA binding 1; HIF-1α, hypoxia-inducible factor-1 alpha; I/R, ischemia-reperfusion; TECs, tubular epithelial cells.

Mentions: Immunohistochemical staining was applied to determine the location of ID1 and HIF-1α expression. As expected, ID1 was mainly expressed in the cytoplasm of renal TECs and was strongly expressed after reperfusion for 2 and 12 hours (Figure 2(a)). HIF-1α was mainly expressed in TECs, in both the cytoplasm and the nucleus. The elevated expression of HIF-1α was observed after reperfusion for 2 hours (Figure 2(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)

Location of ID1 and HIF-1α expression in I/R-injured rat kidney tissue. Immunohistochemical staining for ID1 and HIF-1α in the kidney tissue of I/R and sham-operated rats. (a) Increased staining for ID1 in renal TECs after 2, 6, 12, and 24 hours of reperfusion. (b) Increased staining for HIF-1α in renal TECs after 2 hours of reperfusion. Original magnification, ×200. ID1, inhibitor of DNA binding 1; HIF-1α, hypoxia-inducible factor-1 alpha; I/R, ischemia-reperfusion; TECs, tubular epithelial cells.
© Copyright Policy
Related In: Results  -  Collection

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

fig2: Location of ID1 and HIF-1α expression in I/R-injured rat kidney tissue. Immunohistochemical staining for ID1 and HIF-1α in the kidney tissue of I/R and sham-operated rats. (a) Increased staining for ID1 in renal TECs after 2, 6, 12, and 24 hours of reperfusion. (b) Increased staining for HIF-1α in renal TECs after 2 hours of reperfusion. Original magnification, ×200. ID1, inhibitor of DNA binding 1; HIF-1α, hypoxia-inducible factor-1 alpha; I/R, ischemia-reperfusion; TECs, tubular epithelial cells.
Mentions: Immunohistochemical staining was applied to determine the location of ID1 and HIF-1α expression. As expected, ID1 was mainly expressed in the cytoplasm of renal TECs and was strongly expressed after reperfusion for 2 and 12 hours (Figure 2(a)). HIF-1α was mainly expressed in TECs, in both the cytoplasm and the nucleus. The elevated expression of HIF-1α was observed after reperfusion for 2 hours (Figure 2(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