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1.
Gene Ther ; 17(3): 305-14, 2010 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-20010629

RESUMO

In 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.


Assuntos
Fibroblastos/transplante , Terapia Genética/métodos , Infarto do Miocárdio/terapia , Transgenes , Fatores de Crescimento do Endotélio Vascular/genética , Animais , Fibrina/administração & dosagem , Fibroblastos/metabolismo , Masculino , Infarto do Miocárdio/prevenção & controle , Traumatismo por Reperfusão Miocárdica/prevenção & controle , Traumatismo por Reperfusão Miocárdica/terapia , Neovascularização Fisiológica/genética , Ratos , Ratos Endogâmicos Lew
2.
Sao Paulo Med J ; 115(5): 1548-52, 1997.
Artigo em Inglês | MEDLINE | ID: mdl-9609074

RESUMO

The hemophagocytic syndrome (HS) is characterized by a clinical picture of fever, hepatosplenomegaly, lymphadenopathy and peripheral pancytopenia. The morphologic hallmark of this syndrome is the phagocytosis of hematopoietic elements by morphologically normal macrophages. HS is considered rare and may be a primary disease or associated to viral, infection, neoplasias or autoimmune diseases. Treatment is controversial and its evolution is often fatal. Anatomo-pathological evaluation shows the phenomenon of hemophagocytosis in several organs, especially the hematopoietic tissues. We describe a case of HS, discuss its possible causes, its clinical and pathologic features, its pathophysiology and therapeutic possibilities.


Assuntos
Histiocitose de Células não Langerhans/patologia , Adulto , Evolução Fatal , Humanos , Masculino , Síndrome
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