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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.)

Angiotensin-(1-7) reduces cardiac effects of thyroid hormone by GSK3 beta/NFATc3 signaling pathway

Texto completo
Senger, Nathalia [1] ; Melo, Marcos Barrouin [2] ; Diniz, Gabriela Placona [1] ; Campagnole-Santos, Maria Jose [2] ; Souza Santos, Robson Augusto [2] ; Barreto-Chaves, Maria Luiza M. [1]
Número total de Autores: 6
Afiliação do(s) autor(es):
[1] Univ Sao Paulo, Dept Anat, Sao Paulo - Brazil
[2] Univ Fed Minas Gerais, Dept Physiol & Biophys, Belo Horizonte, MG - Brazil
Número total de Afiliações: 2
Tipo de documento: Artigo Científico
Fonte: Clinical Science; v. 132, n. 11, p. 1117-1133, JUN 14 2018.
Citações Web of Science: 1

Patients with hyperthyroidism exhibit increased risk of development and progression of cardiac diseases. The activation of the renin-angiotensin system (RAS) has been indirectly implicated in these cardiac effects observed in hyperthyroidism. Angiotensin-(1-7) (Ang-(1-7)) has previously been shown to counterbalance pathological effects of angiotensin II (Ang II). The aim of the present study was to investigate the effects of elevated circulating Ang-(1-7) levels on cardiac effects promoted by hyperthyroidism in a transgenic rat (TG) model that constitutively overexpresses an Ang-(1-7)-producing fusion protein {[}TGR(A1-7) 3292]. TG and wild-type (WT) rats received daily injections (i.p.) of triiodothyronine (T3; 7 mu g/100 g of body weight (BW)) or vehicle for 14 days. In contrast withWTrats, the TG rats did not develop cardiac hypertrophy after T3 treatment. Indeed, TG rats displayed reduced systolic blood pressure (SBP) and cardiac hyperdynamic condition induced by hyperthyroidism. Moreover, increased plasma levels of Ang II observed in hyperthyroid WT rats were prevented in TG rats. TG rats were protected from glycogen synthase kinase 3 ss (GSK3 ss) inactivation and nuclear factor of activated T cells (NFAT) nuclear accumulation induced by T3. In vitro studies evidenced that Ang-(1-7) prevented cardiomyocyte hypertrophy and GSK3 ss inactivation induced by T3. Taken together, these data reveal an important cardioprotective action of Ang-(1-7) in experimental model of hyperthyroidism. (AU)

Processo FAPESP: 13/16348-6 - Avaliação do papel terapêutico da angiotensina 1-7 na prevenção dos efeitos cardiovasculares induzidos pelo hormônio tireoidiano em Ratos Wistar
Beneficiário:Nathalia Senger
Linha de fomento: Bolsas no Brasil - Mestrado