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Doctoral Thesis
DOI
10.11606/T.42.2016.tde-09082016-100628
Document
Author
Full name
Ana Paula Cremasco Takano
Institute/School/College
Knowledge Area
Date of Defense
Published
São Paulo, 2016
Supervisor
Committee
Chaves, Maria Luiza Morais Barreto de (President)
Araújo, Ronaldo de Carvalho
Câmara, Niels Olsen Saraiva
Giannocco, Gisele
Munhoz, Carolina Demarchi
Title in Portuguese
Fatores relacionados à inflamação na hipertrofia cardíaca induzida pelo hormônio tiroideano. Contribuição do sistema renina-angiotensina.
Keywords in Portuguese
Cardiomiócito
Hipertrofia cardíaca
Hormônio tiroideano
Inflamação
NF-κB
Sistema renina-angiotensina
Abstract in Portuguese
O presente estudo avaliou aspectos relacionados ao contexto inflamatório na hipertrofia cardíaca induzida pelos hormônios tiroideanos (HT) e o possível envolvimento do sistema renina-angiotensina (SRA) nesse processo, utilizando análises in vivo e com enfoque maior na abordagem in vitro. Os resultados mostraram algumas alterações em citocinas circulantes e cardíacas de animais tratados com HT. Além disso, as expressões de S100A8 e MyD88 foram aumentadas no coração de ratos submetidos ao hipertiroidismo e em cardiomiócitos em cultura estimulados com HT. S100A8 e MyD88 mediaram a ativação do fator nuclear NF-κB pelos HT, tendo papel crucial para o crescimento hipertrófico de cardiomiócitos tratados com HT. Por fim, a ação dos HT modulando a expressão de S100A8 e NF-κB foi mediada pelo SRA. Estes dados contribuem com o entendimento das bases moleculares da ação dos HT e da relação deste com o SRA na hipertrofia cardíaca.
Title in English
Inflammation-related aspects in cardiac hypertrophy induced by thyroid hormone. Contribution of the renin-angiotensin system.
Keywords in English
Cardiac hypertrophy
Cardiomyocyte
Inflammation
NF-κB
Renin- angiotensin system
Thyroid hormone
Abstract in English
The present study evaluated inflammation related aspects in cardiac hypertrophy induced by thyroid hormones (TH) and the possible involvement of the renin-angiotensin system (RAS) in this process, by using in vivo and in vitro analysis. The results showed alterations in circulating and cardiac cytokines from TH treated animals. The expression of S100A8 and MyD88 were increased in the heart of hyperthyroid rats and in cultured cardiomyocytes stimulated with TH. S100A8 and MyD88 mediated the nuclear factor NF-κB activation by TH and these factors presented crucial role to the hypertrophic growth of TH-treated cardiomyocytes. Finally, the action of TH on S100A8 and NF-κB expression was mediated by RAS. These data contribute to the knowledge of molecular basis of TH action and the relationship between TH and RAS in cardiac hypertrophy.
 
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Release Date
2018-08-09
Publishing Date
2016-08-09
 
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