Cardiac gene expression and systemic cytokine profile are complementary in a murine model of post ischemic heart failure

ABSTRACT: After myocardial infarction (MI) activation of the immune system and inflammatory mechanisms, among others, can lead to ventricular remodeling and heart failure (HF). 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. Ischemic HF significantly increased the levels of serum IgM (by 5.2 fold) and IgG (by 3.6 fold) associated with remarkable content of anti-heart specificity. Comparable increase was observed in levels of circulating pro-inflammatory cytokines, such as IL-1β (3.8x) and TNF-α (6.0x). IFN-gamma was also increased in the MI group by 3.1x. However, IL-4 and IL-10 showed no significant difference between MI and sham groups. Chemokines such as MCP-1 and IL-8 were enhanced in the plasma of infarcted mice. We identified 2079 well annotated unigenes that were significantly regulated by the post-ischemic HF. Complement activation and immune response was among the most up-regulated processes. Interestingly, 21 out of the 101 quantified unigenes involved in 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE18703 | GEO | 2009/10/24

SECONDARY ACCESSION(S): PRJNA121493

REPOSITORIES: GEO