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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.)

AT1 receptor blockage impairs NF-kappa B activation mediated by thyroid hormone in cardiomyocytes

Texto completo
Cremasco Takano, Ana Paula [1] ; Senger, Nathalia [1] ; Munhoz, Carolina Demarchi [2] ; Morais Barreto-Chaves, Maria Luiza [1]
Número total de Autores: 4
Afiliação do(s) autor(es):
[1] Univ Sao Paulo, Lab Cellular Biol & Funct Anat, Inst Biomed Sci, Dept Anat, Ave Prof Lineu Prestes 2415, BR-05508000 Sao Paulo, SP - Brazil
[2] Univ Sao Paulo, Inst Biomed Sci, Dept Pharmacol, Sao Paulo, SP - Brazil
Número total de Afiliações: 2
Tipo de documento: Artigo Científico
Fonte: PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY; v. 470, n. 3, p. 549-558, MAR 2018.
Citações Web of Science: 1

We have previously demonstrated that calcium-binding protein S100A8 and myeloid differentiation factor-88 (MyD88) are important mediators of nuclear transcription factor kappa-B (NF-kappa B) activation in cardiomyocytes and that signalling molecules are involved in the hypertrophic response that is stimulated by thyroid hormones (TH). Angiotensin II (Ang II), the main active peptide of the renin-angiotensin system (RAS), binds to type 1 Ang II receptor (AT1R) and subsequently promotes cardiac hypertrophy and the inflammatory response with NF-kappa B activation underlying the cardiovascular effects. Considering the amount of evidence that RAS is an important mediator of TH actions on the cardiovascular system, we aimed to investigate whether cardiac expression of NF-kappa B and upstream associated molecules could be altered in hyperthyroidism, as well as whether AT1R could mediate the effects of TH on cardiac tissue and in cardiomyocytes in culture. Wistar rats were subjected to hyperthyroidism with or without the AT1R blocker losartan. The TH serum levels, haemodynamic parameters and cardiac mass were assessed to confirm the hyperthyroid status. The S100A8, MyD88 and nuclear NF-kappa B expression levels were increased in the hearts of the hyperthyroid rats, and the losartan treatment attenuated these TH effects. In addition, the cultured cardiomyocytes that had been stimulated with losartan exhibited blunted S100A8 upregulation and NF-kappa B activation compared with the TH-treated cells. Together, our results suggest that AT1R participates in TH-induced cardiac hypertrophy partly by mediating S100A8, MyD88 and NF-kappa B activation via TH. These findings indicate the important crosstalk between TH and RAS, highlighting the participation of AT1R in the triggered mechanisms of TH that contribute to the cardiac hypertrophy response. (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: 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