Novel lncRNA XLOC_032768 protects against renal tubular epithelial cells apoptosis in renal ischemia-reperfusion injury by regulating FNDC3B/TGF-β1

被引:9
作者
Zhou, Xiangjun [1 ]
Li, Yongwei [2 ]
Wu, Cheng [1 ]
Yu, Weimin [1 ]
Cheng, Fan [1 ]
机构
[1] Wuhan Univ, Dept Urol, Renmin Hosp, Wuhan 430060, Peoples R China
[2] Qingdao Univ, Affiliated Yantai Yuhuangding Hosp, Dept Urol, Yantai, Peoples R China
基金
中国国家自然科学基金;
关键词
Acute renal injury; ischemia-reperfusion; hypoxia; cell death; lncRNA; NONCODING RNA MALAT1; MESENCHYMAL TRANSITION; KIDNEY; LANDSCAPE;
D O I
10.1080/0886022X.2020.1818579
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
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 inductionin 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-beta 1 and apoptosis of renal tubular cells. Thus, XLOC_032768/FNDC3B/TGF-beta 1signaling pathway in ischemia-reperfusion injury may be targeted for therapy.
引用
收藏
页码:994 / 1003
页数:10
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