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

• Autor(a) principal: Teixeira, Rayane Brinck
• Data de Publicação: 2018
• Outros Autores: Barboza, Tatiana Evelyn, Araújo, Carla Cristina de, Siqueira, Rafaela, Castro, Alexandre Luz de, Bonetto, Jéssica Hellen Poletto, Seolin, Bruna Gazzi de Lima, Carraro, Cristina Campos, Belló-Klein, Adriane, Singal, Pawan K., Araújo, Alex Sander da Rosa
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UFRGS
• Texto Completo: http://hdl.handle.net/10183/188512
• topic: Hipertireoidismo; Cardiomegalia; Morte celular; Inflamação; Cardiac hypertrophy; Cell death; Hyperthyroidism; Inflammation; PGC1-a

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-a, TNF-a, MyD88, p-NFjB, NFjB, p-p38, and p38. Reduced expression of p53 and PGC1-a 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-a 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.