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首页> 外文期刊>Renal failure. >Novel lncRNA XLOC_032768 protects against renal tubular epithelial cells apoptosis in renal ischemia–reperfusion injury by regulating FNDC3B/TGF-β1
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Novel lncRNA XLOC_032768 protects against renal tubular epithelial cells apoptosis in renal ischemia–reperfusion injury by regulating FNDC3B/TGF-β1

机译:新型LNCRNA XLOC_032768通过调节FNDC3B / TGF-β1,防止肾小管上皮细胞凋亡肾缺血再灌注损伤细胞凋亡

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摘要

Renal ischemia–reperfusion injury is a leading cause of acute kidney injury, but its underlying mechanism remains poorly understood and effective therapies are still lacking. Here, we identified lncRNA XLOC_032768 as a novel target in renal ischemia–reperfusion injury by analyzing differentially expressed genes of the transcriptome data. PCR results show that XLOC_032768 was markedly downregulated in the kidney during renal ischemia–reperfusion in mice and in cultured kidney cells during hypoxia. Upon induction in?vitro, XLOC_032768 overexpression repressed the expression of fibronectin type III domain containing 3B (FNDC3B) and tubular epithelial cells apoptosis. Administration of XLOC_032768 preserved FNDC3B expression and attenuated renal tubular epithelial cells apoptosis, resulting in protection against kidney injury in mice. Knockdown of FNDC3B markedly reduced the expression of TGF-β1 and apoptosis of renal tubular cells. Thus, XLOC_032768/FNDC3B/TGF-β1signaling pathway in ischemia–reperfusion injury may be targeted for therapy.
机译:肾缺血再灌注损伤是急性肾损伤的主要原因,但其潜在的机制仍然仍然令人难以理解,有效的疗法仍然缺乏。这里,通过分析转录组数据的差异表达基因,我们将LNCRNA XLOC_032768鉴定为肾缺血再灌注损伤的新靶。 PCR结果表明,XLOC_032768在小鼠肾脏缺血再灌注和缺氧期间培养的肾细胞肾脏缺血再灌注中明显下调。在诱导体外,XLOC_032768过表达抑制含有3B(FNDC3B)和管状上皮细胞凋亡的纤连蛋白III结构域的表达。 XLOC_032768保存的FNDC3B表达和减毒肾小管上皮细胞凋亡,导致小鼠肾损伤的保护。 FNDC3B的敲低明显降低了TGF-β1和肾小管细胞凋亡的表达。因此,缺血再灌注损伤中的XLOC_032768 / FNDC3B / TGF-β1Signaling途径可以靶向治疗。

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