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Войти в исследования Shock (Augusta, Ga.) · 2020
MiR-433 Regulates Myocardial Ischemia Reperfusion Injury by Targeting NDRG4 Via the PI3K/Akt Pathway.
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Cheng Hua, Yan Wei
Аннотация
BACKGROUND AND PURPOSE: Myocardial ischemia reperfusion (IR) injury is a serious issue in the treatment of myocardial infarction. MiR-433 is upregulated in myocardial IR injury, but its specific effects remain unclear. In this study, we explored the effect and mechanism of miR-433 in myocardial IR injury.
METHODS: The expression of miR-433 was measured by qRT-PCR. H9c2 cells were transfected with miR-433 mimic and inhibitor after exposure to HR, respectively. Cell viability was detected by MTT. Cell apoptosis was measured by flow cytometry. Protein expression was assessed by western blot. Dual-luciferase reporter assay was performed to assess the target reaction between miR-433 and NDRG4. In vivo rat model of IR was used, and antagomiR-433 was injected to IR rats.
RESULTS: The qRT-PCR results showed that miR-433 expression increased in H9c2 cardiomyocytes after exposure to HR. Transfection with miR-433 inhibitor significantly increased cell viability, reduced LDH and apoptosis, downregulated Bax level, and upregulated Bcl-2 level. In contrast, the miR-433 mimic significantly augmented the HR-induced effects. Dual-luciferase reporter assay and western blot analysis suggested that miR-433 directly targeted NDRG4. NDRG4 silencing abrogated the protection of miR-433 inhibition on HR injury in H9c2 cells. It also reversed PI3K/Akt pathway activation that was induced by miR-433 inhibition. MiR-433 inhibition significantly decreased CK-MB and LDH serum level in IR rats. And NDRG4, p-PI3K, and p-Akt protein expression was elevated by antagomiR-433 injection in vivo.
CONCLUSION: MiR-433 regulated myocardial IR injury by targeting NDRG4 and modulating PI3K/Akt signal pathway.
METHODS: The expression of miR-433 was measured by qRT-PCR. H9c2 cells were transfected with miR-433 mimic and inhibitor after exposure to HR, respectively. Cell viability was detected by MTT. Cell apoptosis was measured by flow cytometry. Protein expression was assessed by western blot. Dual-luciferase reporter assay was performed to assess the target reaction between miR-433 and NDRG4. In vivo rat model of IR was used, and antagomiR-433 was injected to IR rats.
RESULTS: The qRT-PCR results showed that miR-433 expression increased in H9c2 cardiomyocytes after exposure to HR. Transfection with miR-433 inhibitor significantly increased cell viability, reduced LDH and apoptosis, downregulated Bax level, and upregulated Bcl-2 level. In contrast, the miR-433 mimic significantly augmented the HR-induced effects. Dual-luciferase reporter assay and western blot analysis suggested that miR-433 directly targeted NDRG4. NDRG4 silencing abrogated the protection of miR-433 inhibition on HR injury in H9c2 cells. It also reversed PI3K/Akt pathway activation that was induced by miR-433 inhibition. MiR-433 inhibition significantly decreased CK-MB and LDH serum level in IR rats. And NDRG4, p-PI3K, and p-Akt protein expression was elevated by antagomiR-433 injection in vivo.
CONCLUSION: MiR-433 regulated myocardial IR injury by targeting NDRG4 and modulating PI3K/Akt signal pathway.