AMPK signaling pathway is rapidly activated by T3 and regulates the cardiomyocyte growth
Contribuinte(s) |
UNIVERSIDADE DE SÃO PAULO |
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Data(s) |
14/03/2014
14/03/2014
25/08/2013
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Resumo |
Previous studies have indicated that AMP-activated protein kinase (AMPK) plays a critical role in the control of cardiac hypertrophy mediated by different stimuli such as thyroid hormone (TH). Although the classical effects of TH mediating cardiac hypertrophy occur by transcriptional mechanisms, recent studies have identified other responses to TH, which are more rapid and take place in seconds or minutes evidencing that TH rapidly modulates distinct signaling pathway, which might contribute to the regulation of cardiomyocyte growth. Here, we evaluated the rapid effects of TH on AMPK signaling pathway in cultured cardiomyocytes and determined the involvement of AMPK in T3-induced cardiomyocyte growth. We found for the first time that T3 rapidly activated AMPK signaling pathway. The use of small interfering RNA against AMPK resulted in increased cardiomyocyte hypertrophy while the pharmacological stimulation of AMPK attenuated this process, demonstrating that AMPK contributes to regulation of T3-induced cardiomyocyte growth. Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP, São Paulo Research Foundation - 2009/16888-5) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP, São Paulo Research Foundation - 2009/09922-2) Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq, National Council for Scientific and Technological Development) |
Identificador |
Molecular and Cellular Endocrinology, Limerick, v.376, n.1-2, p.43-50, 2013 http://www.producao.usp.br/handle/BDPI/44129 10.1016/j.mce.2013.05.024 |
Idioma(s) |
eng |
Publicador |
North Holland Publishing Limerick |
Relação |
Molecular and Cellular Endocrinology |
Direitos |
restrictedAccess 2013 Elsevier Ireland Ltd. |
Palavras-Chave | #AMPK #Cardiomyocyte hypertrophy #Thyroid hormone #Hormônios tireoidianos #Proteínas quinases |
Tipo |
article original article publishedVersion |