BMP4 Induces Cardiomyocyte Hypertrophy Through the Activation of ERK 1/2 Signaling Pathway in H9c2 Cells

Detalhes bibliográficos
Autor(a) principal: Yuan,Yu
Data de Publicação: 2019
Outros Autores: Tao,Yezheng, Deng,Yongzhi, Ye,Qunhui, Lin,Bin, Wu,Lin
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Brazilian Archives of Biology and Technology
Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1516-89132019000100315
Resumo: Abstract Bone morphogenetic protein-4 (BMP4) is a member of the bone morphogenetic protein family which plays an important role in bone formation, inflammation and cardiac hypertrophy. The aim of this study was to investigate the underlying molecular mechanism that BMP4-induced cardiomyocyte hypertrophy. H9c2 cells were used to measure cell surface area and protein synthesis. Western blot was used to examine hypertrophic marker brain natriuretic peptide (BNP) protein expression and phosphorylation of ERK1/2. The results exhibited that cell surface area, protein synthesis and BNP protein expression were increased with BMP4 treatment. While PD98059 inhibited these effects of BMP4. In addition, BMP4 treatment increased phosphorylation of ERK1/2 in a time- and dose-dependent manner. PD98059 treatment decreased phosphorylation of ERK1/2 that was increased by BMP4. These results suggest that BMP4 induces cardiomyocyte hypertrophy through the activation of ERK1/2 cell signaling pathway.
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spelling BMP4 Induces Cardiomyocyte Hypertrophy Through the Activation of ERK 1/2 Signaling Pathway in H9c2 CellsBMP4myocardial hypertrophyERK1/2 signaling pathwayAbstract Bone morphogenetic protein-4 (BMP4) is a member of the bone morphogenetic protein family which plays an important role in bone formation, inflammation and cardiac hypertrophy. The aim of this study was to investigate the underlying molecular mechanism that BMP4-induced cardiomyocyte hypertrophy. H9c2 cells were used to measure cell surface area and protein synthesis. Western blot was used to examine hypertrophic marker brain natriuretic peptide (BNP) protein expression and phosphorylation of ERK1/2. The results exhibited that cell surface area, protein synthesis and BNP protein expression were increased with BMP4 treatment. While PD98059 inhibited these effects of BMP4. In addition, BMP4 treatment increased phosphorylation of ERK1/2 in a time- and dose-dependent manner. PD98059 treatment decreased phosphorylation of ERK1/2 that was increased by BMP4. These results suggest that BMP4 induces cardiomyocyte hypertrophy through the activation of ERK1/2 cell signaling pathway.Instituto de Tecnologia do Paraná - Tecpar2019-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S1516-89132019000100315Brazilian Archives of Biology and Technology v.62 2019reponame:Brazilian Archives of Biology and Technologyinstname:Instituto de Tecnologia do Paraná (Tecpar)instacron:TECPAR10.1590/1678-4324-2019180699info:eu-repo/semantics/openAccessYuan,YuTao,YezhengDeng,YongzhiYe,QunhuiLin,BinWu,Lineng2019-12-12T00:00:00Zoai:scielo:S1516-89132019000100315Revistahttps://www.scielo.br/j/babt/https://old.scielo.br/oai/scielo-oai.phpbabt@tecpar.br||babt@tecpar.br1678-43241516-8913opendoar:2019-12-12T00:00Brazilian Archives of Biology and Technology - Instituto de Tecnologia do Paraná (Tecpar)false
dc.title.none.fl_str_mv BMP4 Induces Cardiomyocyte Hypertrophy Through the Activation of ERK 1/2 Signaling Pathway in H9c2 Cells
title BMP4 Induces Cardiomyocyte Hypertrophy Through the Activation of ERK 1/2 Signaling Pathway in H9c2 Cells
spellingShingle BMP4 Induces Cardiomyocyte Hypertrophy Through the Activation of ERK 1/2 Signaling Pathway in H9c2 Cells
Yuan,Yu
BMP4
myocardial hypertrophy
ERK1/2 signaling pathway
title_short BMP4 Induces Cardiomyocyte Hypertrophy Through the Activation of ERK 1/2 Signaling Pathway in H9c2 Cells
title_full BMP4 Induces Cardiomyocyte Hypertrophy Through the Activation of ERK 1/2 Signaling Pathway in H9c2 Cells
title_fullStr BMP4 Induces Cardiomyocyte Hypertrophy Through the Activation of ERK 1/2 Signaling Pathway in H9c2 Cells
title_full_unstemmed BMP4 Induces Cardiomyocyte Hypertrophy Through the Activation of ERK 1/2 Signaling Pathway in H9c2 Cells
title_sort BMP4 Induces Cardiomyocyte Hypertrophy Through the Activation of ERK 1/2 Signaling Pathway in H9c2 Cells
author Yuan,Yu
author_facet Yuan,Yu
Tao,Yezheng
Deng,Yongzhi
Ye,Qunhui
Lin,Bin
Wu,Lin
author_role author
author2 Tao,Yezheng
Deng,Yongzhi
Ye,Qunhui
Lin,Bin
Wu,Lin
author2_role author
author
author
author
author
dc.contributor.author.fl_str_mv Yuan,Yu
Tao,Yezheng
Deng,Yongzhi
Ye,Qunhui
Lin,Bin
Wu,Lin
dc.subject.por.fl_str_mv BMP4
myocardial hypertrophy
ERK1/2 signaling pathway
topic BMP4
myocardial hypertrophy
ERK1/2 signaling pathway
description Abstract Bone morphogenetic protein-4 (BMP4) is a member of the bone morphogenetic protein family which plays an important role in bone formation, inflammation and cardiac hypertrophy. The aim of this study was to investigate the underlying molecular mechanism that BMP4-induced cardiomyocyte hypertrophy. H9c2 cells were used to measure cell surface area and protein synthesis. Western blot was used to examine hypertrophic marker brain natriuretic peptide (BNP) protein expression and phosphorylation of ERK1/2. The results exhibited that cell surface area, protein synthesis and BNP protein expression were increased with BMP4 treatment. While PD98059 inhibited these effects of BMP4. In addition, BMP4 treatment increased phosphorylation of ERK1/2 in a time- and dose-dependent manner. PD98059 treatment decreased phosphorylation of ERK1/2 that was increased by BMP4. These results suggest that BMP4 induces cardiomyocyte hypertrophy through the activation of ERK1/2 cell signaling pathway.
publishDate 2019
dc.date.none.fl_str_mv 2019-01-01
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1516-89132019000100315
url http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1516-89132019000100315
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv 10.1590/1678-4324-2019180699
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv text/html
dc.publisher.none.fl_str_mv Instituto de Tecnologia do Paraná - Tecpar
publisher.none.fl_str_mv Instituto de Tecnologia do Paraná - Tecpar
dc.source.none.fl_str_mv Brazilian Archives of Biology and Technology v.62 2019
reponame:Brazilian Archives of Biology and Technology
instname:Instituto de Tecnologia do Paraná (Tecpar)
instacron:TECPAR
instname_str Instituto de Tecnologia do Paraná (Tecpar)
instacron_str TECPAR
institution TECPAR
reponame_str Brazilian Archives of Biology and Technology
collection Brazilian Archives of Biology and Technology
repository.name.fl_str_mv Brazilian Archives of Biology and Technology - Instituto de Tecnologia do Paraná (Tecpar)
repository.mail.fl_str_mv babt@tecpar.br||babt@tecpar.br
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