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

Autor(es)

Cremasco Takano, Ana Paula ; Munhoz, Carolina Demarchi ; Moriscot, Anselmo Sigari ; Gupta, Sudhiranjan ; Morais Barreto-Chaves, Maria Luiza

• 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: 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
• Modalidade de apoio: Bolsas no Brasil - Doutorado
• Processo FAPESP: 15/01166-5 - Efeito da inibição de NF-kB na hipertrofia cardíaca induzida pelo hormônio tiroideano
• Beneficiário: Ana Paula Cremasco Takano
• Modalidade de apoio: Bolsas no Exterior - Estágio de Pesquisa - 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
• Modalidade de apoio: Auxílio à Pesquisa - Regular