Erythropoietin helix B surface peptide modulates miR-21/Atg12 axis to alleviates cardiomyocyte hypoxia-reoxygenation injury.
Am J Transl Res
; 11(4): 2422-2430, 2019.
Article
em En
| MEDLINE
| ID: mdl-31105848
ABSTRACT
BACKGROUND:
The erythropoietin helix B surface peptide (HBSP) has been shown to have neuroprotective and repair-damaging myocardium effects similar to erythropoietin (EPO). However, the protective mechanism of HBSP on cardiomyocyte hypoxia-reoxygenation (H/R) injury is not clear.METHODS:
H9C2 cells were pretreated with HBSP and subjected to hypoxia/reoxygenation (H/R), changes in cell function, autophagy and apoptosis were assessed, respectively. Cells were transfected with miR-21 mimic and miR-NC, and the relative expression of miR-21 and Atg12 were detected by qRT-PCR. The target role of miR-21 and Atg12 was evaluated by dual-luciferase reporter. After transfected with si-Atg12 and si-NC, western blot was used to assess autophagy and apoptosis proteins, flow cytometry assay was used to detect apoptosis rate.RESULTS:
We found the expression of miR-21 was significantly down-regulated, accompanied by remarkably activated of autophagy and apoptosis in H9C2 cells during H/R injury. Pleasantly, HBSP pretreatment has a similar effect as transfection of miR-21 mimic, which is to evidently inhibit autophagy and apoptosis by up-regulating miR-21 expression. Moreover, Bioinformatics analysis and luciferase reporter assay revealed that Atg12 was directly bond to miR-21. To further understand whether Atg12 is involved in the process of miR-21 regulating autophagy, si-Atg12 and si-NC were transfected into H9C2 cell, the results showed that knockdown of Atg12 enhances the inhibition autophagy and apoptosis effect of HBSP.CONCLUSION:
These results demonstrate that HBSP inhibits myocardial H/R injury induced by autophagy over-activation and apoptosis via miR-21/Atg12 axis.
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Base de dados:
MEDLINE
Idioma:
En
Ano de publicação:
2019
Tipo de documento:
Article