Decreased PGC1-α levels and increased apoptotic protein signaling are associated with the maladaptive cardiac hypertrophy in hyperthyroidism
Autor(a) principal: | |
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Data de Publicação: | 2018 |
Outros Autores: | , , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UFRGS |
Texto Completo: | http://hdl.handle.net/10183/188512 |
Resumo: | 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. |
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Teixeira, Rayane BrinckBarboza, Tatiana EvelynAraújo, Carla Cristina deSiqueira, RafaelaCastro, Alexandre Luz deBonetto, Jéssica Hellen PolettoSeolin, Bruna Gazzi de LimaCarraro, Cristina CamposBelló-Klein, AdrianeSingal, Pawan K.Araújo, Alex Sander da Rosa2019-02-02T02:31:33Z20180973-7138http://hdl.handle.net/10183/188512001083242Hyperthyroidism 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.application/pdfengJournal of biosciences. [Bangalore]. Vol. 43, no. 5 (Dec. 2018), p. 887–895HipertireoidismoCardiomegaliaMorte celularInflamaçãoCardiac hypertrophyCell deathHyperthyroidismInflammationPGC1-aDecreased PGC1-α levels and increased apoptotic protein signaling are associated with the maladaptive cardiac hypertrophy in hyperthyroidismEstrangeiroinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFRGSinstname:Universidade Federal do Rio Grande do Sul (UFRGS)instacron:UFRGSTEXT001083242.pdf.txt001083242.pdf.txtExtracted Texttext/plain34503http://www.lume.ufrgs.br/bitstream/10183/188512/2/001083242.pdf.txt25db163e06e820d69338ebdf8398875cMD52ORIGINAL001083242.pdfTexto completo (inglês)application/pdf1008186http://www.lume.ufrgs.br/bitstream/10183/188512/1/001083242.pdf2b3b9251d62d4d57335167c3194bd3d0MD5110183/1885122019-03-03 02:29:01.924191oai:www.lume.ufrgs.br:10183/188512Repositório de PublicaçõesPUBhttps://lume.ufrgs.br/oai/requestopendoar:2019-03-03T05:29:01Repositório Institucional da UFRGS - Universidade Federal do Rio Grande do Sul (UFRGS)false |
dc.title.pt_BR.fl_str_mv |
Decreased PGC1-α levels and increased apoptotic protein signaling are associated with the maladaptive cardiac hypertrophy in hyperthyroidism |
title |
Decreased PGC1-α levels and increased apoptotic protein signaling are associated with the maladaptive cardiac hypertrophy in hyperthyroidism |
spellingShingle |
Decreased PGC1-α levels and increased apoptotic protein signaling are associated with the maladaptive cardiac hypertrophy in hyperthyroidism Teixeira, Rayane Brinck Hipertireoidismo Cardiomegalia Morte celular Inflamação Cardiac hypertrophy Cell death Hyperthyroidism Inflammation PGC1-a |
title_short |
Decreased PGC1-α levels and increased apoptotic protein signaling are associated with the maladaptive cardiac hypertrophy in hyperthyroidism |
title_full |
Decreased PGC1-α levels and increased apoptotic protein signaling are associated with the maladaptive cardiac hypertrophy in hyperthyroidism |
title_fullStr |
Decreased PGC1-α levels and increased apoptotic protein signaling are associated with the maladaptive cardiac hypertrophy in hyperthyroidism |
title_full_unstemmed |
Decreased PGC1-α levels and increased apoptotic protein signaling are associated with the maladaptive cardiac hypertrophy in hyperthyroidism |
title_sort |
Decreased PGC1-α levels and increased apoptotic protein signaling are associated with the maladaptive cardiac hypertrophy in hyperthyroidism |
author |
Teixeira, Rayane Brinck |
author_facet |
Teixeira, Rayane Brinck 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 |
author_role |
author |
author2 |
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 |
author2_role |
author author author author author author author author author author |
dc.contributor.author.fl_str_mv |
Teixeira, Rayane Brinck 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 |
dc.subject.por.fl_str_mv |
Hipertireoidismo Cardiomegalia Morte celular Inflamação |
topic |
Hipertireoidismo Cardiomegalia Morte celular Inflamação Cardiac hypertrophy Cell death Hyperthyroidism Inflammation PGC1-a |
dc.subject.eng.fl_str_mv |
Cardiac hypertrophy Cell death Hyperthyroidism Inflammation PGC1-a |
description |
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. |
publishDate |
2018 |
dc.date.issued.fl_str_mv |
2018 |
dc.date.accessioned.fl_str_mv |
2019-02-02T02:31:33Z |
dc.type.driver.fl_str_mv |
Estrangeiro info:eu-repo/semantics/article |
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info:eu-repo/semantics/publishedVersion |
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publishedVersion |
dc.identifier.uri.fl_str_mv |
http://hdl.handle.net/10183/188512 |
dc.identifier.issn.pt_BR.fl_str_mv |
0973-7138 |
dc.identifier.nrb.pt_BR.fl_str_mv |
001083242 |
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url |
http://hdl.handle.net/10183/188512 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.ispartof.pt_BR.fl_str_mv |
Journal of biosciences. [Bangalore]. Vol. 43, no. 5 (Dec. 2018), p. 887–895 |
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info:eu-repo/semantics/openAccess |
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openAccess |
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