Odanacatib Inhibits Resistin-induced Hypertrophic H9c2 Cardiomyoblast Cells Through LKB1/AMPK Pathway
Autor(a) principal: | |
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Data de Publicação: | 2017 |
Outros Autores: | , , , , , |
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=S1516-89132017000100309 |
Resumo: | ABSTRACT Odanacatib (ODN) is a selective inhibitor of cathepsin K. The cysteine protease cathepsin K has been implicated in cardiac hypertrophy. Resistine is an adipokine which is identified to promote cardiac hypertrophy. Here, we hypothesize that ODN mitigates resistin-induced myocyte hypertrophy. Cell surface area and protein synthesis were measured after treatment with resistin and ODN in H9c2 cells. The expression of cardiomyocyte hypertrophy marker BNP and β-MHC was detected by RT-qPCR. The expression and phosphorylation of AMPK and LKB1 were analyzed with Western blot. Resistin could significantly increase cardiomyocyte cell surface area, protein synthesis, and embryonic gene BNP and β-MHC expression, inhibit phosphorylation of AMPK and LKB1. ODN could significantly reverse the effects of resistin. Collectively, our data suggest that ODN can inhibit cardiomyocyte hypertrophy induced by resistin and the underlying mechanism may be involved in LKB1/AMPK pathway. |
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Brazilian Archives of Biology and Technology |
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Odanacatib Inhibits Resistin-induced Hypertrophic H9c2 Cardiomyoblast Cells Through LKB1/AMPK PathwayResistinOdanacatibLKB1/AMPK pathwayCardiomyocyte hypertrophyABSTRACT Odanacatib (ODN) is a selective inhibitor of cathepsin K. The cysteine protease cathepsin K has been implicated in cardiac hypertrophy. Resistine is an adipokine which is identified to promote cardiac hypertrophy. Here, we hypothesize that ODN mitigates resistin-induced myocyte hypertrophy. Cell surface area and protein synthesis were measured after treatment with resistin and ODN in H9c2 cells. The expression of cardiomyocyte hypertrophy marker BNP and β-MHC was detected by RT-qPCR. The expression and phosphorylation of AMPK and LKB1 were analyzed with Western blot. Resistin could significantly increase cardiomyocyte cell surface area, protein synthesis, and embryonic gene BNP and β-MHC expression, inhibit phosphorylation of AMPK and LKB1. ODN could significantly reverse the effects of resistin. Collectively, our data suggest that ODN can inhibit cardiomyocyte hypertrophy induced by resistin and the underlying mechanism may be involved in LKB1/AMPK pathway.Instituto de Tecnologia do Paraná - Tecpar2017-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S1516-89132017000100309Brazilian Archives of Biology and Technology v.60 2017reponame:Brazilian Archives of Biology and Technologyinstname:Instituto de Tecnologia do Paraná (Tecpar)instacron:TECPAR10.1590/1678-4324-2017160333info:eu-repo/semantics/openAccessZheng,XianLiu,HuziCheng,GuanchangLuo,JianweiYe,QunhuiDeng,YongzhiWu,Lineng2018-12-03T00:00:00Zoai:scielo:S1516-89132017000100309Revistahttps://www.scielo.br/j/babt/https://old.scielo.br/oai/scielo-oai.phpbabt@tecpar.br||babt@tecpar.br1678-43241516-8913opendoar:2018-12-03T00:00Brazilian Archives of Biology and Technology - Instituto de Tecnologia do Paraná (Tecpar)false |
dc.title.none.fl_str_mv |
Odanacatib Inhibits Resistin-induced Hypertrophic H9c2 Cardiomyoblast Cells Through LKB1/AMPK Pathway |
title |
Odanacatib Inhibits Resistin-induced Hypertrophic H9c2 Cardiomyoblast Cells Through LKB1/AMPK Pathway |
spellingShingle |
Odanacatib Inhibits Resistin-induced Hypertrophic H9c2 Cardiomyoblast Cells Through LKB1/AMPK Pathway Zheng,Xian Resistin Odanacatib LKB1/AMPK pathway Cardiomyocyte hypertrophy |
title_short |
Odanacatib Inhibits Resistin-induced Hypertrophic H9c2 Cardiomyoblast Cells Through LKB1/AMPK Pathway |
title_full |
Odanacatib Inhibits Resistin-induced Hypertrophic H9c2 Cardiomyoblast Cells Through LKB1/AMPK Pathway |
title_fullStr |
Odanacatib Inhibits Resistin-induced Hypertrophic H9c2 Cardiomyoblast Cells Through LKB1/AMPK Pathway |
title_full_unstemmed |
Odanacatib Inhibits Resistin-induced Hypertrophic H9c2 Cardiomyoblast Cells Through LKB1/AMPK Pathway |
title_sort |
Odanacatib Inhibits Resistin-induced Hypertrophic H9c2 Cardiomyoblast Cells Through LKB1/AMPK Pathway |
author |
Zheng,Xian |
author_facet |
Zheng,Xian Liu,Huzi Cheng,Guanchang Luo,Jianwei Ye,Qunhui Deng,Yongzhi Wu,Lin |
author_role |
author |
author2 |
Liu,Huzi Cheng,Guanchang Luo,Jianwei Ye,Qunhui Deng,Yongzhi Wu,Lin |
author2_role |
author author author author author author |
dc.contributor.author.fl_str_mv |
Zheng,Xian Liu,Huzi Cheng,Guanchang Luo,Jianwei Ye,Qunhui Deng,Yongzhi Wu,Lin |
dc.subject.por.fl_str_mv |
Resistin Odanacatib LKB1/AMPK pathway Cardiomyocyte hypertrophy |
topic |
Resistin Odanacatib LKB1/AMPK pathway Cardiomyocyte hypertrophy |
description |
ABSTRACT Odanacatib (ODN) is a selective inhibitor of cathepsin K. The cysteine protease cathepsin K has been implicated in cardiac hypertrophy. Resistine is an adipokine which is identified to promote cardiac hypertrophy. Here, we hypothesize that ODN mitigates resistin-induced myocyte hypertrophy. Cell surface area and protein synthesis were measured after treatment with resistin and ODN in H9c2 cells. The expression of cardiomyocyte hypertrophy marker BNP and β-MHC was detected by RT-qPCR. The expression and phosphorylation of AMPK and LKB1 were analyzed with Western blot. Resistin could significantly increase cardiomyocyte cell surface area, protein synthesis, and embryonic gene BNP and β-MHC expression, inhibit phosphorylation of AMPK and LKB1. ODN could significantly reverse the effects of resistin. Collectively, our data suggest that ODN can inhibit cardiomyocyte hypertrophy induced by resistin and the underlying mechanism may be involved in LKB1/AMPK pathway. |
publishDate |
2017 |
dc.date.none.fl_str_mv |
2017-01-01 |
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=S1516-89132017000100309 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1516-89132017000100309 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1590/1678-4324-2017160333 |
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.60 2017 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 |
_version_ |
1750318277832212480 |