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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.)

S100A8/MYD88/NF-O > B: a novel pathway involved in cardiomyocyte hypertrophy driven by thyroid hormone

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Autor(es):
Cremasco Takano, Ana Paula ; Munhoz, Carolina Demarchi ; Moriscot, Anselmo Sigari ; Gupta, Sudhiranjan ; Morais Barreto-Chaves, Maria Luiza
Número total de Autores: 5
Tipo de documento: Artigo Científico
Fonte: JOURNAL OF MOLECULAR MEDICINE-JMM; v. 95, n. 6, p. 671-682, JUN 2017.
Citações Web of Science: 4
Resumo

Recent studies have evidenced the involvement of inflammation-related pathways to the development of cardiac hypertrophy and other consequences on the cardiovascular system, including the calcium-binding protein S100A8. However, this has never been investigated in the thyroid hormone (TH)-prompted cardiac hypertrophy. Thus, we aimed to test whether S100A8 and related signaling molecules, myeloid differentiation factor-88 (MyD88) and nuclear factor kappa B (NF-kappa B), could be associated with the cardiomyocyte hypertrophy induced by TH. Our results demonstrate that the S100A8/MyD88/NF-kappa B signaling pathway is activated in cardiomyocytes following TH stimulation. The knockdown of S100A8 and MyD88 indicates the contribution of those molecules to cardiomyocyte hypertrophy in response to TH, as evaluated by cell surface area, leucine incorporation assay, and gene expression. Furthermore, S100A8 and MyD88 are crucial mediators of NF-kappa B activation, which is also involved in the hypertrophic growth of TH-treated cardiomyocytes. Supporting the in vitro data, the contribution of NF-kappa B for TH-induced cardiac hypertrophy is confirmed in vivo, by using transgenic mice with cardiomyocyte-specific suppression of NF-kappa B. These data identify a novel pathway regulated by TH that mediates cardiomyocyte hypertrophy. However, the potential role of this new pathway in short and long-term cardiac effects of TH remains to be further investigated. (AU)

Processo FAPESP: 15/01166-5 - Efeito da inibição de NF-kB na hipertrofia cardíaca induzida pelo hormônio tiroideano
Beneficiário:Ana Paula Cremasco Takano
Linha de fomento: Bolsas no Exterior - Estágio de Pesquisa - Doutorado
Processo FAPESP: 11/23352-4 - Associação entre vias relacionadas à inflamação e à hipertrofia cardíaca induzida pelo hormônio tiroideano. papel do sistema renina-angiotensina
Beneficiário:Ana Paula Cremasco Takano
Linha de fomento: Bolsas no Brasil - Doutorado
Processo FAPESP: 13/22480-4 - Inflamação e hipertrofia cardíaca induzida por hormônio tiroideano: papel do sistema renina-angiotensina
Beneficiário:Maria Luiza de Morais Barreto de Chaves
Linha de fomento: Auxílio à Pesquisa - Regular