Please use this identifier to cite or link to this item: https://www.arca.fiocruz.br/handle/icict/30450
Title: Cardiac gene expression and systemic cytokine profile are complementary in a murine model of post-ischemic heart failure
Authors: Lachtermacher, S.
Esporcatte, B. L. B.
Montalvão, F.
Costa, P. C.
Rodrigues, D. C.
Belem, L.
Rabischoffisky, A.
Faria Neto, Hugo C. C.
Vasconcellos, R.
Iacobas, S.
Dohmann, H. F. R.
Spray, D. C.
Goldenberg, R. C. S.
Carvalho, A. C. Campos de
Affilliation: Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil.
Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil.
Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil.
Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil.
Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil.
Centro de Ensino e Pesquisa, Hospital Pró-Cardíaco, Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Fisiologia e Farmacodinâmica. Rio de Janeiro, RJ, Brasil.
Universidade Federal Fluminense. Instituto de Imunologia. Departamento de Imunobiologia. Niterói, RJ. Brasil.
Albert Einstein College of Medicine. Bronx, NY, USA.
Albert Einstein College of Medicine. Bronx, NY, USA.
Centro de Ensino e Pesquisa, Hospital Pró-Cardíaco, Rio de Janeiro, RJ, Brasil.
Albert Einstein College of Medicine. Bronx, NY, USA.
Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil.
Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil / Albert Einstein College of Medicine. Bronx, NY, USA.
Abstract: After myocardial infarction (MI), activation of the immune system and inflammatory mechanisms, among others, can lead to ventricular remodeling and heart failure (HF). The interaction between these systemic alterations and corresponding changes in the heart has not been extensively examined in the setting of chronic ischemia. The main purpose of this study was to investigate alterations in cardiac gene and systemic cytokine profile in mice with post-ischemic HF. Plasma was tested for IgM and IgG anti-heart reactive repertoire and inflammatory cytokines. Heart samples were assayed for gene expression by analyzing hybridization to AECOM 32k mouse microarrays. Ischemic HF significantly increased the levels of total serum IgM (by 5.2-fold) and total IgG (by 3.6-fold) associated with a relatively high content of anti-heart specificity. A comparable increase was observed in the levels of circulating pro-inflammatory cytokines such as IL-1β (3.8X) and TNF-α (6.0X). IFN-γ was also increased by 3.1-fold in the MI group. However, IL-4 and IL-10 were not significantly different between the MI and sham-operated groups. Chemokines such as MCP-1 and IL-8 were 1.4- and 13-fold increased, respectively, in the plasma of infarcted mice. We identified 2079 well annotated unigenes that were significantly regulated by post-ischemic HF. Complement activation and immune response were among the most up-regulated processes. Interestingly, 21 of the 101 quantified unigenes involved in the inflammatory response were significantly up-regulated and none were down-regulated. These data indicate that post-ischemic heart remodeling is accompanied by immune-mediated mechanisms that act both systemically and locally.
Keywords: Experimental post-ischemic heart failure
Anti-heart antibodies
Cytokines
Immunoarray
RNAm - Microarray
keywords: Insuficiência cardíaca pós-isquêmica experimental
Anticorpos anti-coração
Citocinas
DeCS: RNA Mensageiro
Issue Date: 2010
Publisher: Associação Brasileira de Divulgação Científica
Citation: LACHTERMACHER, S. et al. Cardiac gene expression and systemic cytokine profile are complementary in a murine model of post-ischemic heart failure. Brazilian Journal of Medical and Biological Research, v.43, p.377-389, 2010.
ISSN: 0100-879X
Copyright: open access
Appears in Collections:IOC - Artigos de Periódicos

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