The Bone Morphogenetic Protein Antagonist Gremlin Promotes Vascular Smooth Muscle Cell Apoptosis

Detalhes bibliográficos
Autor(a) principal: Maciel, Thiago Trovati [UNIFESP]
Data de Publicação: 2009
Outros Autores: Melo, Rosilene Santos [UNIFESP], Campos, Alexandre Holthausen [UNIFESP]
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNIFESP
Texto Completo: http://repositorio.unifesp.br/handle/11600/31134
http://dx.doi.org/10.1159/000189793
Resumo: Background: Previous studies from our laboratory demonstrated that gremlin significantly increases vascular smooth muscle cell (VSMC) proliferation and migration. the present study investigates gremlin expression in the initial stages of rat carotid balloon injury and its effects on VSMC apoptosis. Methods: Gremlin mRNA expression was evaluated in rat carotids and cultured VSMCs by quantitative PCR. Apoptosis was analyzed in A7r5 cells and rabbit primary VSMCs following gremlin gene overexpression or silencing by chromatin morphology and caspase-3 activity. Results: Vascular injury promoted a significant decrease in gremlin mRNA levels. in addition, platelet-derived growth factor, angiotensin II and transforming growth factor (TGF)-beta 1 promoted coordinated regulation of gremlin and bone morphogenetic protein (BMP)-4 expression in opposite directions according to the confluence status of VSMC culture. in A7r5 cells, gremlin overexpression was able to increase apoptosis, as demonstrated by chromatin morphology and caspase-3 activity, while BMP administration promoted opposite effects. Finally, in agreement with our results, gremlin gene silencing effectively suppressed apoptosis in A7r5 cells and rabbit VSMCs. Conclusion: Gremlin is regulated by growth factors and vascular injury and is involved in modulation of VSMC apoptosis. Modifications of gremlin expression during vascular injury may contribute to the apoptosis resistance of VSMCs. Copyright (C) 2009 S. Karger AG, Basel
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spelling Maciel, Thiago Trovati [UNIFESP]Melo, Rosilene Santos [UNIFESP]Campos, Alexandre Holthausen [UNIFESP]Universidade Federal de São Paulo (UNIFESP)2016-01-24T13:52:01Z2016-01-24T13:52:01Z2009-01-01Journal of Vascular Research. Basel: Karger, v. 46, n. 4, p. 325-332, 2009.1018-1172http://repositorio.unifesp.br/handle/11600/31134http://dx.doi.org/10.1159/00018979310.1159/000189793WOS:000267091200007Background: Previous studies from our laboratory demonstrated that gremlin significantly increases vascular smooth muscle cell (VSMC) proliferation and migration. the present study investigates gremlin expression in the initial stages of rat carotid balloon injury and its effects on VSMC apoptosis. Methods: Gremlin mRNA expression was evaluated in rat carotids and cultured VSMCs by quantitative PCR. Apoptosis was analyzed in A7r5 cells and rabbit primary VSMCs following gremlin gene overexpression or silencing by chromatin morphology and caspase-3 activity. Results: Vascular injury promoted a significant decrease in gremlin mRNA levels. in addition, platelet-derived growth factor, angiotensin II and transforming growth factor (TGF)-beta 1 promoted coordinated regulation of gremlin and bone morphogenetic protein (BMP)-4 expression in opposite directions according to the confluence status of VSMC culture. in A7r5 cells, gremlin overexpression was able to increase apoptosis, as demonstrated by chromatin morphology and caspase-3 activity, while BMP administration promoted opposite effects. Finally, in agreement with our results, gremlin gene silencing effectively suppressed apoptosis in A7r5 cells and rabbit VSMCs. Conclusion: Gremlin is regulated by growth factors and vascular injury and is involved in modulation of VSMC apoptosis. Modifications of gremlin expression during vascular injury may contribute to the apoptosis resistance of VSMCs. Copyright (C) 2009 S. Karger AG, BaselFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Albert Einstein Research and Education InstituteUniversidade Federal de São Paulo, Albert Einstein Res & Educ Inst, BR-05651901 São Paulo, BrazilUniversidade Federal de São Paulo, Div Nephrol, BR-05651901 São Paulo, BrazilUniversidade Federal de São Paulo, Div Nephrol, EPM, BR-05651901 São Paulo, BrazilFAPESP: 06/00456-0Web of Science325-332engKargerJournal of Vascular Researchhttp://www.karger.com/Services/RightsPermissionsinfo:eu-repo/semantics/openAccessApoptosisBone morphogenetic proteinsGremlinVascular injuryVascular smooth muscle cellsThe Bone Morphogenetic Protein Antagonist Gremlin Promotes Vascular Smooth Muscle Cell Apoptosisinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlereponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP11600/311342022-11-04 15:13:29.143metadata only accessoai:repositorio.unifesp.br:11600/31134Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652022-11-04T18:13:29Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false
dc.title.en.fl_str_mv The Bone Morphogenetic Protein Antagonist Gremlin Promotes Vascular Smooth Muscle Cell Apoptosis
title The Bone Morphogenetic Protein Antagonist Gremlin Promotes Vascular Smooth Muscle Cell Apoptosis
spellingShingle The Bone Morphogenetic Protein Antagonist Gremlin Promotes Vascular Smooth Muscle Cell Apoptosis
Maciel, Thiago Trovati [UNIFESP]
Apoptosis
Bone morphogenetic proteins
Gremlin
Vascular injury
Vascular smooth muscle cells
title_short The Bone Morphogenetic Protein Antagonist Gremlin Promotes Vascular Smooth Muscle Cell Apoptosis
title_full The Bone Morphogenetic Protein Antagonist Gremlin Promotes Vascular Smooth Muscle Cell Apoptosis
title_fullStr The Bone Morphogenetic Protein Antagonist Gremlin Promotes Vascular Smooth Muscle Cell Apoptosis
title_full_unstemmed The Bone Morphogenetic Protein Antagonist Gremlin Promotes Vascular Smooth Muscle Cell Apoptosis
title_sort The Bone Morphogenetic Protein Antagonist Gremlin Promotes Vascular Smooth Muscle Cell Apoptosis
author Maciel, Thiago Trovati [UNIFESP]
author_facet Maciel, Thiago Trovati [UNIFESP]
Melo, Rosilene Santos [UNIFESP]
Campos, Alexandre Holthausen [UNIFESP]
author_role author
author2 Melo, Rosilene Santos [UNIFESP]
Campos, Alexandre Holthausen [UNIFESP]
author2_role author
author
dc.contributor.institution.none.fl_str_mv Universidade Federal de São Paulo (UNIFESP)
dc.contributor.author.fl_str_mv Maciel, Thiago Trovati [UNIFESP]
Melo, Rosilene Santos [UNIFESP]
Campos, Alexandre Holthausen [UNIFESP]
dc.subject.eng.fl_str_mv Apoptosis
Bone morphogenetic proteins
Gremlin
Vascular injury
Vascular smooth muscle cells
topic Apoptosis
Bone morphogenetic proteins
Gremlin
Vascular injury
Vascular smooth muscle cells
description Background: Previous studies from our laboratory demonstrated that gremlin significantly increases vascular smooth muscle cell (VSMC) proliferation and migration. the present study investigates gremlin expression in the initial stages of rat carotid balloon injury and its effects on VSMC apoptosis. Methods: Gremlin mRNA expression was evaluated in rat carotids and cultured VSMCs by quantitative PCR. Apoptosis was analyzed in A7r5 cells and rabbit primary VSMCs following gremlin gene overexpression or silencing by chromatin morphology and caspase-3 activity. Results: Vascular injury promoted a significant decrease in gremlin mRNA levels. in addition, platelet-derived growth factor, angiotensin II and transforming growth factor (TGF)-beta 1 promoted coordinated regulation of gremlin and bone morphogenetic protein (BMP)-4 expression in opposite directions according to the confluence status of VSMC culture. in A7r5 cells, gremlin overexpression was able to increase apoptosis, as demonstrated by chromatin morphology and caspase-3 activity, while BMP administration promoted opposite effects. Finally, in agreement with our results, gremlin gene silencing effectively suppressed apoptosis in A7r5 cells and rabbit VSMCs. Conclusion: Gremlin is regulated by growth factors and vascular injury and is involved in modulation of VSMC apoptosis. Modifications of gremlin expression during vascular injury may contribute to the apoptosis resistance of VSMCs. Copyright (C) 2009 S. Karger AG, Basel
publishDate 2009
dc.date.issued.fl_str_mv 2009-01-01
dc.date.accessioned.fl_str_mv 2016-01-24T13:52:01Z
dc.date.available.fl_str_mv 2016-01-24T13:52:01Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
format article
status_str publishedVersion
dc.identifier.citation.fl_str_mv Journal of Vascular Research. Basel: Karger, v. 46, n. 4, p. 325-332, 2009.
dc.identifier.uri.fl_str_mv http://repositorio.unifesp.br/handle/11600/31134
http://dx.doi.org/10.1159/000189793
dc.identifier.issn.none.fl_str_mv 1018-1172
dc.identifier.doi.none.fl_str_mv 10.1159/000189793
dc.identifier.wos.none.fl_str_mv WOS:000267091200007
identifier_str_mv Journal of Vascular Research. Basel: Karger, v. 46, n. 4, p. 325-332, 2009.
1018-1172
10.1159/000189793
WOS:000267091200007
url http://repositorio.unifesp.br/handle/11600/31134
http://dx.doi.org/10.1159/000189793
dc.language.iso.fl_str_mv eng
language eng
dc.relation.ispartof.none.fl_str_mv Journal of Vascular Research
dc.rights.driver.fl_str_mv http://www.karger.com/Services/RightsPermissions
info:eu-repo/semantics/openAccess
rights_invalid_str_mv http://www.karger.com/Services/RightsPermissions
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 325-332
dc.publisher.none.fl_str_mv Karger
publisher.none.fl_str_mv Karger
dc.source.none.fl_str_mv reponame:Repositório Institucional da UNIFESP
instname:Universidade Federal de São Paulo (UNIFESP)
instacron:UNIFESP
instname_str Universidade Federal de São Paulo (UNIFESP)
instacron_str UNIFESP
institution UNIFESP
reponame_str Repositório Institucional da UNIFESP
collection Repositório Institucional da UNIFESP
repository.name.fl_str_mv Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)
repository.mail.fl_str_mv
_version_ 1802764184439488512

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