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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

MicroRNA-1 overexpression blunts cardiomyocyte hypertrophy elicited by thyroid hormone

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Autor(es):
Diniz, Gabriela Placona ; Lino, Caroline Antunes ; Moreno, Camila Rodrigues ; Senger, Nathalia ; Morais Barreto-Chaves, Maria Luiza
Número total de Autores: 5
Tipo de documento: Artigo Científico
Fonte: Journal of Cellular Physiology; v. 232, n. 12, p. 3360-3368, DEC 2017.
Citações Web of Science: 6
Resumo

It is well-known that increased thyroid hormone (TH) levels induce cardiomyocyte growth. MicroRNAs (miRNAs) have been identified as key players in cardiomyocyte hypertrophy, which is associated with increased risk of heart failure. In this study, we evaluated the miR-1 expression in TH-induced cardiac hypertrophy, as well as the potential involvement of miR-1 in cardiomyocyte hypertrophy elicited by TH in vitro. The possible role of type 1 angiotensin II receptor (AT1R) in the effect promoted by TH in miR-1 expression was also evaluated. Neonatal rat cardiac myocytes (NRCMs) were treated with T-3 for 24 hr and Wistar rats were subjected to hyperthyroidism for 14 days combined or not with AT1R blocker. Real Time RT-PCR analysis indicated that miR-1 expression was decreased in cardiac hypertrophy in response to TH in vitro and in vivo, and this effect was unchanged by AT1R blocker. In addition, HDAC4, which is target of miR-1, was increased in NRCMs after T-3 treatment. A gain-of-function study revealed that overexpression of miR-1 prevented T-3-induced cardiomyocyte hypertrophy and reduced HADC4mRNA levels in NRCMs. In vivo experiments confirmed the downregulation of miR-1 in cardiac tissue from hyperthyroid animals, which was accompanied by increased HDAC4 mRNA levels. In addition, HDAC inhibitor prevented T-3-induced cardiomyocyte hypertrophy. Our data reveal a new mechanistic insight into cardiomyocyte growth in response to TH, suggesting that miR-1 plays a role in cardiomyocyte hypertrophy induced by TH potentially via targeting HADC4. (AU)

Processo FAPESP: 09/14567-7 - Análise da expressão de microRNAs na hipertrofia cardíaca induzida pelo hormônio tiroideano in vivo e in vitro - participação do receptor AT1
Beneficiário:Gabriela Placoná Diniz
Linha de fomento: Bolsas no Brasil - Pós-Doutorado