Journal of Biosciences

, Volume 43, Issue 5, pp 887–895 | Cite as

Decreased PGC1-α levels and increased apoptotic protein signaling are associated with the maladaptive cardiac hypertrophy in hyperthyroidism

  • Rayane Brinck Teixeira
  • Tatiane Evelyn Barboza
  • Carla Cristina de Araújo
  • Rafaela Siqueira
  • Alexandre Luz de Castro
  • Jéssica Hellen Poletto Bonetto
  • Bruna Gazzi de Lima-Seolin
  • Cristina Campos Carraro
  • Adriane Belló-Klein
  • Pawan K Singal
  • Alex Sander da Rosa AraujoEmail author


Hyperthyroidism can lead to the activation of proteins which are associated with inflammation, apoptosis, hypertrophy, and heart failure. This study aimed to explore the inflammatory and apoptotic proteins involved in the hyperthyroidism-induced cardiac hypertrophy establishment. Male Wistar rats were divided into control and hyperthyroid (12 mg/L L-thyroxine, in drinking water for 28 days) groups. The expression of inflammatory and apoptotic signaling proteins was quantified in the left ventricle by Western blot. Hyperthyroidism was confirmed by evaluation of T3 and T4 levels, as well as cardiac hypertrophy development. There was no change in the expression of HSP70, HIF1-α, TNF-α, MyD88, p-NFκB, NFκB, p-p38, and p38. Reduced expression of p53 and PGC1-α was associated with increased TLR4 and decreased IL-10 expression. Decreased Bcl-2 expression and increased Bax/Bcl-2 ratio were also observed. The results suggest that reduced PGC1-α and IL-10, and elevated TLR4 proteins expression could be involved with the diminished mitochondrial biogenesis and anti-inflammatory response, as well as cell death signaling, in the establishment of hyperthyroidism-induced maladaptive cardiac hypertrophy.


Cardiac hypertrophy cell death hyperthyroidism inflammation PGC1-α 



Veterinary medical support from Dr. André Ricardo Ribeiro Belló is acknowledged. We also acknowledge Professor Ilma Simoni Brum, Physiology Department, UFRGS, for providing the p53 antibody. This paper was written during a scholarship provided by the International Cooperation Program CAPES/DFATD at the University of Manitoba. This study was funded by Conselho Nacional de Desenvolvimento Científico e tecnológico, Fundação de Amparo à Pesquisa do Estado do Rio Grande do Sul and Coordenação de Aperfeiçoamento de Pessoal de Nível Superior.


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Copyright information

© Indian Academy of Sciences 2018

Authors and Affiliations

  • Rayane Brinck Teixeira
    • 1
  • Tatiane Evelyn Barboza
    • 2
  • Carla Cristina de Araújo
    • 1
  • Rafaela Siqueira
    • 1
  • Alexandre Luz de Castro
    • 1
  • Jéssica Hellen Poletto Bonetto
    • 1
  • Bruna Gazzi de Lima-Seolin
    • 1
  • Cristina Campos Carraro
    • 1
  • Adriane Belló-Klein
    • 1
  • Pawan K Singal
    • 3
  • Alex Sander da Rosa Araujo
    • 1
    Email author
  1. 1.Laboratório de Fisiologia Cardiovascular, Departamento de Fisiologia, Instituto de Ciências Básicas da SaúdeUniversidade Federal do Rio Grande do SulPorto AlegreBrazil
  2. 2.Laboratório de Disfunções Cardiovasculares, Departamento de AnatomiaUniversidade de São PauloSão PauloBrazil
  3. 3.Institute of Cardiovascular Sciences, St. Boniface General Hospital Research CentreUniversity of ManitobaWinnipegCanada

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