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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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

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Author(s):
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]
Total Authors: 6
Affiliation:
[1] Univ Sao Paulo, Dept Anat, Sao Paulo - Brazil
[2] Univ Fed Minas Gerais, Dept Physiol & Biophys, Belo Horizonte, MG - Brazil
Total Affiliations: 2
Document type: Journal article
Source: Clinical Science; v. 132, n. 11, p. 1117-1133, JUN 14 2018.
Web of Science Citations: 1
Abstract

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)

FAPESP's process: 13/16348-6 - Evaluation of therapeutic role of Angiotensin 1-7 in the prevention of the cardiovascular effects induced by thyroid hormone in Wistar rats
Grantee:Nathalia Senger
Support Opportunities: Scholarships in Brazil - Master