BACKGROUND: The cytotoxic action of leukocytes is known to be a probable cause of the cardiac myocyte damage seen in idiopathic dilated cardiomyopathy (IDC). Monocyte chemoattractant protein 1 (MCP-1) contributes to enhanced leukocyte recruitment and activation resulting in chronic damage of cardiomyocytes. MCP-1 has been reported to be dynamically regulated in IDC and may contribute to the deterioration of left ventricular function. In addition, a polymorphism at -2518 (G/A) in the MCP-1 gene affects the level of MCP-1 expression in response to an inflammatory stimulus. METHODS AND RESULTS: We genotyped the polymorphism at -2518 G/A in the MCP-1 gene in 73 Japanese patients with nonfamilial IDC and 349 healthy controls. The distribution of the MCP-1 genotypes in the IDC patients differed significantly from the controls (p=0.016). In a dominant G allele model, there was a significant difference in the distribution of genotypes between the two groups (p<0.01). The odds ratio for nonfamilial IDC associated with the GG vs. non-GG genotype was 10.4 (95% CI=1.7-64.5) after adjustment for the confounding factors. CONCLUSIONS: These findings suggest that the G allele at -2518 in the MCP-1 gene may be a novel genetic marker of susceptibility to nonfamilial IDC.
BACKGROUND: The cytotoxic action of leukocytes is known to be a probable cause of the cardiac myocyte damage seen in idiopathic dilated cardiomyopathy (IDC). Monocyte chemoattractant protein 1 (MCP-1) contributes to enhanced leukocyte recruitment and activation resulting in chronic damage of cardiomyocytes. MCP-1 has been reported to be dynamically regulated in IDC and may contribute to the deterioration of left ventricular function. In addition, a polymorphism at -2518 (G/A) in the MCP-1 gene affects the level of MCP-1 expression in response to an inflammatory stimulus. METHODS AND RESULTS: We genotyped the polymorphism at -2518 G/A in the MCP-1 gene in 73 Japanese patients with nonfamilial IDC and 349 healthy controls. The distribution of the MCP-1 genotypes in the IDC patients differed significantly from the controls (p=0.016). In a dominant G allele model, there was a significant difference in the distribution of genotypes between the two groups (p<0.01). The odds ratio for nonfamilial IDC associated with the GG vs. non-GG genotype was 10.4 (95% CI=1.7-64.5) after adjustment for the confounding factors. CONCLUSIONS: These findings suggest that the G allele at -2518 in the MCP-1 gene may be a novel genetic marker of susceptibility to nonfamilial IDC.
Authors: Piotr Piotrowski; Margarita Lianeri; Robert Gasik; Andrzej Roszak; Marzena Olesińska; Paweł P Jagodziński Journal: J Biomed Biotechnol Date: 2010-04-21