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Downregulation of XIST ameliorates acute kidney injury by sponging miR‐142‐5p and targeting PDCD4
Author(s) -
Tang Bo,
Li Weiliang,
Ji Tingting,
Li Xiaoying,
Qu Xiaolei,
Feng Linhong,
Zhu Yingchun,
Qi Yinghui,
Zhu Chun,
Bai Shoujun
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29729
Subject(s) - xist , gene knockdown , downregulation and upregulation , long non coding rna , cancer research , microrna , acute kidney injury , kidney , microbiology and biotechnology , biology , chemistry , medicine , apoptosis , biochemistry , gene , x inactivation , x chromosome
Acute kidney injury (AKI) is a common kidney disease that markedly affects public health. To date, the roles of long noncoding RNA XIST in AKI are poorly understood. Here, we investigated the biological functions of XIST in AKI. We observed that XIST expression increased in patients with AKI and HK‐2 cells stimulated by CoCl 2 . In addition, a rat AKI model induced by ischemia–reperfusion was established. Tumor necrosis factor‐α, interleukin‐6, and cyclooxygenase‐2 messenger RNA expression were induced in vivo; moreover, XIST expression was upregulated. Knockdown of XIST significantly repressed CoCl 2 ‐triggered injury in HK‐2 cells. However, microRNA (miR)‐142‐5p, a downstream target of XIST, was downregulated in AKI. miR‐142‐5p was repressed by XIST and miR‐142‐5p could inhibit CoCl 2 ‐induced injury in HK‐2 cells. Moreover, PDCD4 expression was significantly increased in AKI. PDCD4 was predicted to be the target of miR‐142‐5p. Subsequently, loss of PDCD4 was able to retard injury in HK‐2 cells exposed to CoCl 2. Thus, we suggest that XIST regulates miR‐142‐5p and PDCD4, and it has the potential to function as a biomarker in therapeutic strategies for AKI.