MiR-378 Inhibits Angiotensin II-Induced Cardiomyocyte Hypertrophy by Targeting AKT2.
Int Heart J
; 65(3): 528-536, 2024.
Article
em En
| MEDLINE
| ID: mdl-38825497
ABSTRACT
Cardiomyocyte hypertrophy plays a crucial role in heart failure development, potentially leading to sudden cardiac arrest and death. Previous studies suggest that micro-ribonucleic acids (miRNAs) show promise for the early diagnosis and treatment of cardiomyocyte hypertrophy.To investigate the miR-378 expression in the cardiomyocyte hypertrophy model, reverse transcription-polymerase chain reaction (RT-qPCR), Western blot, and immunofluorescence tests were conducted in angiotensin II (Ang II)-induced H9c2 cells and Ang II-induced mouse model of cardiomyocyte hypertrophy. The functional interaction between miR-378 and AKT2 was studied by dual-luciferase reporter, RNA pull-down, Western blot, and RT-qPCR assays.The results of RT-qPCR analysis showed the downregulated expression of miR-378 in both the cell and animal models of cardiomyocyte hypertrophy. It was observed that the introduction of the miR-378 mimic inhibited the hypertrophy of cardiomyocytes induced by Ang II. Furthermore, the co-transfection of AKT2 expression vector partially mitigated the negative impact of miR-378 overexpression on Ang II-induced cardiomyocytes. Molecular investigations provided evidence that miR-378 negatively regulated AKT2 expression by interacting with the 3' untranslated region (UTR) of AKT2 mRNA.Decreased miR-378 expression and AKT2 activation are linked to Ang II-induced cardiomyocyte hypertrophy. Targeting miR-378/AKT2 axis offers therapeutic opportunity to alleviate cardiomyocyte hypertrophy.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Angiotensina II
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Miócitos Cardíacos
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MicroRNAs
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Proteínas Proto-Oncogênicas c-akt
Limite:
Animals
Idioma:
En
Revista:
Int Heart J
Assunto da revista:
CARDIOLOGIA
Ano de publicação:
2024
Tipo de documento:
Article