Intramyocardial transplantation of fibroblasts expressing vascular endothelial growth factor attenuates cardiac dysfunction

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dc.contributor.authorGonçalves, Giovana Aparecida
dc.contributor.authorVassallo, Paula Frizela
dc.contributor.authorSantos, Leonardo dos
dc.contributor.authorSchettert, Isolmar Tadeu
dc.contributor.authorNakamuta, Juliana Sanajotti
dc.contributor.authorBecker, Claudia
dc.contributor.authorTucci, Paulo José Ferreira [UNIFESP]
dc.contributor.authorKrieger, Jose Eduardo
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2016-01-24T13:59:21Z
dc.date.available2016-01-24T13:59:21Z
dc.date.issued2010-03-01
dc.description.abstractIn this study, we analyzed whether transplantation of cardiac fibroblasts (CFs) expressing vascular endothelial growth factor (VEGF) mitigates cardiac dysfunction after myocardial infarction (MI) in rats. First, we observed that the transgene expression lasts longer (45 vs 7 days) when fibroblasts are used as vectors compared with myoblasts. in a preventive protocol, induction of cardiac neovascularization accompanied by reduction in myocardial scar area was observed when cell transplantation was performed 1 week before ischemia/reperfusion and the animals analyzed 3 weeks later. Finally, the therapeutic efficacy of this approach was tested injecting cells in a fibrin biopolymer, to increase cardiac retention, 24 h post-MI. After 4 weeks, an increase in neovascularization and a decrease in myocardial collagen were observed only in rats that received cells expressing VEGF. Basal indirect or direct hemodynamic measurements showed no differences among the groups whereas under pharmacological stress, only the group that received cells expressing VEGF showed a significant reduction in end-diastolic pressure and improvement in stroke volume and cardiac work. These results indicate that transplantation of CFs expressing VEGF using fibrin biopolymer induces neovascularization and attenuates left ventricle fibrosis and cardiac dysfunction in ischemic heart. Gene Therapy (2010) 17, 305-314; doi:10.1038/gt.2009.146; published online 10 December 2009en
dc.description.affiliationUniv São Paulo, Sch Med, Lab Genet & Mol Cardiol, Heart Inst InCor,Dept Med, BR-05403000 São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Cardiac Physiol & Physiopathol Lab, Dept Physiol, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Cardiac Physiol & Physiopathol Lab, Dept Physiol, São Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt
dc.description.sponsorshipMinistério da Ciência e Tecnologia
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)pt
dc.description.sponsorshipMinistério da Saúde/Departamento Ciência e Tecnologia
dc.description.sponsorshipIDFAPESP: 01/00090pt
dc.description.sponsorshipIDMinistério da Saúde/Departamento Ciência e Tecnologia: 552324/20005-1
dc.description.sponsorshipIDMinistério da Saúde/Departamento Ciência e Tecnologia: 10120104096700
dc.description.sponsorshipIDFAPESP: 04/06784-4pt
dc.description.sponsorshipIDFAPESP: 03/02671-8pt
dc.description.sponsorshipIDFAPESP: 03/02672-4pt
dc.format.extent305-314
dc.identifierhttps://dx.doi.org/10.1038/gt.2009.146
dc.identifier.citationGene Therapy. London: Nature Publishing Group, v. 17, n. 3, p. 305-314, 2010.
dc.identifier.doi10.1038/gt.2009.146
dc.identifier.issn0969-7128
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/32290
dc.identifier.wosWOS:000275392600002
dc.language.isoeng
dc.publisherNature Publishing Group
dc.relation.ispartofGene Therapy
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectGene cell therapyen
dc.subjectVEGFen
dc.subjectAngiogenic growth factorsen
dc.subjectCardiac repairen
dc.subjectAngiogenesis gene therapyen
dc.subjectBiopolymer scaffolden
dc.titleIntramyocardial transplantation of fibroblasts expressing vascular endothelial growth factor attenuates cardiac dysfunctionen
dc.typeinfo:eu-repo/semantics/article
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