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首页> 外文期刊>Transplantation Proceedings >Stable expression of hypoxia-inducible factor-1α in human renal proximal tubular epithelial cells promotes epithelial to mesenchymal transition
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Stable expression of hypoxia-inducible factor-1α in human renal proximal tubular epithelial cells promotes epithelial to mesenchymal transition

机译：缺氧诱导因子-1α在人肾近端肾小管上皮细胞中的稳定表达促进上皮向间质的转化

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Background 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. Methods 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. Results 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. Conclusion 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.
机译：背景技术晚期异体肾移植功能障碍已成为一个重要问题，肾小管萎缩和间质纤维化是主要原因。据报道，缺氧可以诱导肾小管上皮细胞（TECs）的上皮-间质转化（EMT），而缺氧诱导因子1（HIF-1）是细胞适应缺氧的重要调节剂之一。方法在本研究中，我们使用表达HIF-1αΔODD的腺病毒，该腺病毒在常氧条件下可以稳定且功能性地表达HIF-1α，并使用缺氧/复氧细胞模型体外模拟缺血/再灌注（I / R）损伤，研究HIF-1α对EMT相关基因表达的影响。结果我们的结果表明，HIF-1α可以显着上调I / R损伤HK-2细胞中α-平滑肌肌动蛋白的表达，并降低E-钙黏着蛋白的表达。此外，在此过程中，miR-21表达与HIF-1α呈正相关。结论这些结果表明，HIF-1α可能通过调节人肾TEC I / R损伤过程中纤维化基因的表达来促进EMT的发展，而miR-21可能是该过程中的重要调控途径。

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