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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

HIF-1α and vimentin induction in the HK-2 cell H/R model. (a, b) Western blot analysis of HIF-1α and vimentin in HK-2 cells under hypoxia (H) and reoxygenation (R). Cells for reoxygenation experienced 24 hours of hypoxia. β-actin was examined as the loading control. A representative blot from 3 independent experiments is shown. (c, d) Quantitative RT-PCR was used for the analysis of HIF-1α and vimentin mRNA levels in HK-2 cells under H/R. Data are expressed as mean ± SD for HIF-1α and vimentin levels using β-actin mRNA as an internal control (n = 3). ∗P < .05 compared with the prehypoxia controls. HIF-1α, hypoxia-inducible factor-1 alpha; H/R, hypoxia-reoxygenation.
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fig3: HIF-1α and vimentin induction in the HK-2 cell H/R model. (a, b) Western blot analysis of HIF-1α and vimentin in HK-2 cells under hypoxia (H) and reoxygenation (R). Cells for reoxygenation experienced 24 hours of hypoxia. β-actin was examined as the loading control. A representative blot from 3 independent experiments is shown. (c, d) Quantitative RT-PCR was used for the analysis of HIF-1α and vimentin mRNA levels in HK-2 cells under H/R. Data are expressed as mean ± SD for HIF-1α and vimentin levels using β-actin mRNA as an internal control (n = 3). ∗P < .05 compared with the prehypoxia controls. HIF-1α, hypoxia-inducible factor-1 alpha; H/R, hypoxia-reoxygenation.

Mentions: The detailed dynamic expression of HIF-1α and vimentin by western blot (Figures 3(a) and 3(b)) was observed. HIF-1α expression was induced obviously during hypoxia and reduced immediately at the beginning of reoxygenation, followed by a transient induction during reoxygenation. Vimentin expression was increased gradually and significantly upregulated during the reoxygenation phase. qRT-PCR was performed to estimate the mRNA levels of HIF-1α and vimentin (Figures 3(c) and 3(d)). The HIF-1α mRNA levels were significantly changed during the latter half of hypoxia and reoxygenation. In addition, there was an upregulation of vimentin at the transcription level.


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)

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

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

fig3: HIF-1α and vimentin induction in the HK-2 cell H/R model. (a, b) Western blot analysis of HIF-1α and vimentin in HK-2 cells under hypoxia (H) and reoxygenation (R). Cells for reoxygenation experienced 24 hours of hypoxia. β-actin was examined as the loading control. A representative blot from 3 independent experiments is shown. (c, d) Quantitative RT-PCR was used for the analysis of HIF-1α and vimentin mRNA levels in HK-2 cells under H/R. Data are expressed as mean ± SD for HIF-1α and vimentin levels using β-actin mRNA as an internal control (n = 3). ∗P < .05 compared with the prehypoxia controls. HIF-1α, hypoxia-inducible factor-1 alpha; H/R, hypoxia-reoxygenation.
Mentions: The detailed dynamic expression of HIF-1α and vimentin by western blot (Figures 3(a) and 3(b)) was observed. HIF-1α expression was induced obviously during hypoxia and reduced immediately at the beginning of reoxygenation, followed by a transient induction during reoxygenation. Vimentin expression was increased gradually and significantly upregulated during the reoxygenation phase. qRT-PCR was performed to estimate the mRNA levels of HIF-1α and vimentin (Figures 3(c) and 3(d)). The HIF-1α mRNA levels were significantly changed during the latter half of hypoxia and reoxygenation. In addition, there was an upregulation of vimentin at the transcription level.

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