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miR‐370 promotes high glucose‐induced podocyte injuries by inhibiting angiotensin II type 1 receptor‐associated protein
Author(s) -
Xian Yuxin,
Dong Liping,
Jia Yong,
Lin Yi,
Jiao Wenjuan,
Wang Yao
Publication year - 2018
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.11048
Subject(s) - podocyte , propidium iodide , annexin , apoptosis , microrna , chemistry , microbiology and biotechnology , blot , fluorescein isothiocyanate , angiotensin ii , receptor , annexin a2 , cancer research , biology , endocrinology , gene , biochemistry , programmed cell death , kidney , physics , quantum mechanics , proteinuria , fluorescence
Abstract miRNAs expression profiles in podocyte injuries have been reported in different models in vivo and in vitro. In the present study, miR‐370 was elevated in high glucose‐stimulated podocyte, and the post‐transcriptional mechanism of miR‐370 was investigated in high glucose‐induced podocyte injuries. The gene and protein levels were assayed by RT‐qPCR and Western blotting, respectively. Annexin V‐fluorescein isothiocyanate (FITC)/propidium iodide (PI) staining was used to evaluate the apoptosis in high glucose‐stimulated podocyte. The targeted genes were predicted by a bioinformatics algorithm and confirmed by a dual luciferase reporter assay. The results demonstrated that over‐activation of miR‐370 was verified in high glucose‐treated podocytes, while miR‐370 repression protected against high glucose‐induced apoptosis, cell membrane, and DNA damage in podocytes. We also found that AGTRAP as a direct target of miR‐370 served as an opposite effect to miR‐370, and overexpression of AGTRAP blocked high glucose‐induced podocytes dysfunction. In conclusions, high glucose‐induced podocytes damage by activating miR‐370 signaling targeted to inhibit the expression of AGTRAP, representing a novel and promising therapeutic target for the treatment of DN.