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• W2011427135 abstract "Late kidney allograft dysfunction is becoming a significant problem and tubular atrophy and interstitial fibrosis are main causes. It was reported that hypoxia could induce epithelial—mesenchymal transition (EMT) in renal tubular epithelial cells (TECs), and hypoxia-inducible factor-1 (HIF-1) is one of the important regulators of cellular adaptive to hypoxia. In this study, we used an HIF-1αΔODD–expressing adenovirus, which could stably and functionally express HIF-1α under normoxia conditions, and used a hypoxia/reoxygenation cell model to simulate ischemia/reperfusion (I/R) injury in vitro, to investigate the effect of HIF-1α on EMT-related gene expressions. Our results demonstrated that HIF-1α could significantly upregulate α-smooth muscle actin expression, and reduced the E-cadherin expression in HK-2 cells during I/R injury. Moreover, miR-21 expression had a positive correlation with HIF-1α in this process. These results suggest that HIF-1α may promote the EMT development through regulating fibrotic gene expression during I/R injury in human renal TECs, and miR-21 could be among the important regulatory pathways in the process." @default.
• W2011427135 created "2016-06-24" @default.
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• W2011427135 date "2014-01-01" @default.
• W2011427135 modified "2023-09-23" @default.
• W2011427135 title "Stable Expression of Hypoxia-Inducible Factor-1α in Human Renal Proximal Tubular Epithelial Cells Promotes Epithelial to Mesenchymal Transition" @default.
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• W2011427135 doi "https://doi.org/10.1016/j.transproceed.2013.06.024" @default.
• W2011427135 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24507038" @default.
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