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MEG3 aggravates hypoxia/reoxygenation induced apoptosis of renal tubular epithelial cells via the miR‐129‐5p/HMGB1 axis
Author(s) -
Mao Huihui,
Huang Qiao,
Liu Ying
Publication year - 2021
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.22649
Subject(s) - apoptosis , meg3 , flow cytometry , downregulation and upregulation , gene knockdown , chemistry , viability assay , microbiology and biotechnology , western blot , cell culture , cell , reporter gene , gene expression , cancer research , biology , long non coding rna , gene , biochemistry , genetics
The apoptosis of renal tubular epithelial cells (TECs) during ischemia/reperfusion (I/R) facilitates the progression of acute kidney injury (AKI). This study aimed to probe the role of long noncoding RNA maternally expressed 3 (MEG3) in I/R‐induced apoptosis of TECs. In this study, with CoCl 2 and hypoxia/reoxygenation treatments, cell models were established to mimic I/R using the human kidney tubular cell line HK‐2. In HK‐2 cells, expression of MEG3 detected using quantitative real‐time polymerase chain reaction (qRT‐PCR), was significantly upregulated after CoCl 2 treatment and hypoxia/reoxygenation treatment. The results of cell counting kit‐8 assay and flow cytometry suggested that knockdown of MEG3 significantly increased the viability of HK‐2 cells but inhibited its apoptosis, while overexpression of MEG3 exerted the reverse effects. Additionally, expression levels of interleukin 6 and tumor necrosis factor‐α in the medium were elevated after MEG3 was overexpressed in HK‐2 cells. Together with qRT‐PCR and Western blot analysis, a dual‐luciferase reporter gene assay was used to verify the interactions among MEG3, miR‐129‐5p, and HMGB1. The results demonstrated that in HK‐2 cells, miR‐129‐5p was a target of MEG3, and HMGB1 served as a target gene of miR‐129‐5p. Besides this, compared with the control group, the expression levels of MEG3 and HMGB1 in samples derived from AKI patients were remarkably upregulated, and the expression of miR‐129‐5p was downregulated. Therefore, taken together, we conclude that the overexpression of MEG3 induced by I/R promotes apoptosis of TECs via regulating the miR‐129‐5p/HMGB1 axis.