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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.)

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

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Author(s):
Cremasco Takano, Ana Paula [1] ; Senger, Nathalia [1] ; Munhoz, Carolina Demarchi [2] ; Morais Barreto-Chaves, Maria Luiza [1]
Total Authors: 4
Affiliation:
[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
Total Affiliations: 2
Document type: Journal article
Source: PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY; v. 470, n. 3, p. 549-558, MAR 2018.
Web of Science Citations: 1
Abstract

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)

FAPESP's process: 11/23352-4 - Association between inflammation-related pathways and cardiac hypertrophy induced by thyroid hormone. role of the renin-angiotensin system
Grantee:Ana Paula Cremasco Takano
Support type: Scholarships in Brazil - Doctorate
FAPESP's process: 13/22480-4 - Inflammation and cardiac hypertrophy induced by thyroid hormones: contribution of renin-angiotensin system
Grantee:Maria Luiza de Morais Barreto de Chaves
Support type: Regular Research Grants