Short-term myocardial ischemia induces cardiac mCRP expression and pro-inflammatory gene (Cox-2, MCP-1, and TF) up-regulation in peripheral blood mononuclear cells.
2008, J Thromb Haemost. 2008 Nov 25.
Vilahur G, Hernández-Vera R, Molins B, Casaní L, Duran X, Padró T, Badimon L.
Related authors of the center Badimon Lina, Casaní Laura, Padró Teresa, Vilahur Gemma, Hernández Rodrigo.
Vilahur G, Hernández-Vera R, Molins B, Casaní L, Duran X, Padró T, Badimon L.
Related authors of the center Badimon Lina, Casaní Laura, Padró Teresa, Vilahur Gemma, Hernández Rodrigo.
Cardiovascular Research Center, CSIC-ICCC, Hospital de la Santa Creu i Sant Pau, Barcelona.
Background: Prompt coronary thrombus resolution, reducing time of ischemia, improves cardiac recovery. The factors triggered by ischemia that contribute to the clinical outcome are not fully known. We hypothesize that unabated inflammation due to cardiac ischemia may be a contributing factor. Aims: As a proof-of-concept we evaluated the effect of short-term myocardial ischemia on the local and systemic inflammatory response. Methods: Pigs either underwent 90min mid-LAD balloon occlusion (infarct size 25+/-1% left ventricle; 29% heart function deterioration) or a sham-operation procedure. Peri-infarcted and non-ischemic cardiac tissue was obtained for histopathological, molecular, and immunohistochemical analysis of inflammatory markers (IL-6, TNF-alpha, mCRP, and HAM-56). Blood (femoral vein) was withdrawn prior MI-induction (t=0) and at 30 and 90min to evaluate: 1)systemic cytokine levels (IL-6, TNF-alpha, CRP; 2)pro-inflammatory gene and protein expression in peripheral blood mononuclear cells (PBMC) of TF, Cox-2, MCP-1, and CRP; and 3)platelet activation (assessed by perfusion studies and RhoA activation). Results: Short-term ischemia triggered cardiac IL-6 and TNF-alpha expression, recruitment of inflammatory cells, and mCRP expression in infiltrated macrophages (p<0.05 vs t=0 and sham). PBMC mRNA and protein expression of MCP-1, Cox-2, and TF was significantly increased by ischemia whereas no differences were detected in CRP. Ischemia increased cTroponin-I, IL-6 and TNF-alpha systemic levels and was associated with higher platelet deposition and RhoA activation (P<0.001 vs t=0 and sham). Conclusion: Short-term myocardial ischemia, even without atherosclerosis, induces an inflammatory phenotype by inducing local recruitment of macrophages and a systemic activation of mononuclear cells and renders platelets more susceptible to activation.
PMID: 19036073 [PubMed - as supplied by publisher]
Background: Prompt coronary thrombus resolution, reducing time of ischemia, improves cardiac recovery. The factors triggered by ischemia that contribute to the clinical outcome are not fully known. We hypothesize that unabated inflammation due to cardiac ischemia may be a contributing factor. Aims: As a proof-of-concept we evaluated the effect of short-term myocardial ischemia on the local and systemic inflammatory response. Methods: Pigs either underwent 90min mid-LAD balloon occlusion (infarct size 25+/-1% left ventricle; 29% heart function deterioration) or a sham-operation procedure. Peri-infarcted and non-ischemic cardiac tissue was obtained for histopathological, molecular, and immunohistochemical analysis of inflammatory markers (IL-6, TNF-alpha, mCRP, and HAM-56). Blood (femoral vein) was withdrawn prior MI-induction (t=0) and at 30 and 90min to evaluate: 1)systemic cytokine levels (IL-6, TNF-alpha, CRP; 2)pro-inflammatory gene and protein expression in peripheral blood mononuclear cells (PBMC) of TF, Cox-2, MCP-1, and CRP; and 3)platelet activation (assessed by perfusion studies and RhoA activation). Results: Short-term ischemia triggered cardiac IL-6 and TNF-alpha expression, recruitment of inflammatory cells, and mCRP expression in infiltrated macrophages (p<0.05 vs t=0 and sham). PBMC mRNA and protein expression of MCP-1, Cox-2, and TF was significantly increased by ischemia whereas no differences were detected in CRP. Ischemia increased cTroponin-I, IL-6 and TNF-alpha systemic levels and was associated with higher platelet deposition and RhoA activation (P<0.001 vs t=0 and sham). Conclusion: Short-term myocardial ischemia, even without atherosclerosis, induces an inflammatory phenotype by inducing local recruitment of macrophages and a systemic activation of mononuclear cells and renders platelets more susceptible to activation.
PMID: 19036073 [PubMed - as supplied by publisher]
Catalan Institute of Cardiovascular Sciences
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