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Effect of miR‐499a‐5p on damage of cardiomyocyte induced by hypoxia‐reoxygenation via downregulating CD38 protein
Author(s) -
Zhao Lei,
Wang BaoHua,
Zhang WeiJia,
Sun LiXia
Publication year - 2020
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.29334
Subject(s) - apoptosis , chemistry , western blot , flow cytometry , hypoxia (environmental) , microbiology and biotechnology , lactate dehydrogenase , cd38 , luciferase , blot , biochemistry , gene , biology , enzyme , transfection , oxygen , stem cell , organic chemistry , cd34
The aim is to investigate the mechanism of miR‐499a‐5p on the damage of cardiomyocyte induced by hypoxia/reoxygenation. The activity of lactate dehydrogenase (LDH), apoptosis rate and the expression of miR‐499a‐5p and cluster of differentiation 38 (CD38) in hypoxia‐reoxygenation model cells were detected by LDH Cytotoxicity Assay Kit, flow cytometry, real‐time polymerase chain reaction, and Western blot analysis, respectively. Apoptosis, the activity of LDH was detected after overexpression of miR‐499a‐5p or silencing of CD38 in H9c2 cells. The target relationship between miR‐499a‐5p and CD38 was verified by Targetscan online prediction and dual‐luciferase assay. Apoptosis, the activity of LDH was detected after overexpression of miR‐499a‐5p and CD38. Apoptosis, the activity of LDH and the expression of CD38 were increased ( P < .05) while expression of miR‐499a‐5p was decreased ( P < .05) in hypoxia/reoxygenation model cells. Apoptosis and the activity of LDH in H9c2 cells after overexpression of miR‐499a‐5p or silence of CD38 were decreased ( P < .05). The results of Targetscan online prediction and dual‐luciferase assay indicated that CD38 was a potential target gene of miR‐499a‐5p. Overexpression of CD38 could reverse the inhibition of miR‐499a‐5p on LDH activity and apoptosis in H9c2 cells. miR‐499a‐5p could relief the injury of cardiomyocytes induced by hypoxia/reoxygenation via targeting CD38.