Key result
CCL2 SNPs and serum MCP-1 levels are not linked to future CAD risk.
Why the study?
Evidence about the association between MCP-1 levels, CCL2 genetic variants, and risk of coronary artery disease is contradictory.
Are CCL2 genetic variants and serum MCP-1 levels associated with the risk of future coronary artery disease in apparently healthy adults?
Case-Control (n=3,375)
Are CCL2 genetic variants and serum MCP-1 levels associated with the risk of future coronary artery disease in apparently healthy adults?
This study found no evidence to support the hypothesis that MCP-1 levels or CCL2 genetic variants are associated with the development of coronary artery disease, challenging previous publications.
No association found between CCL2 variants or MCP-1 levels and CAD; challenges prior reports but leaves the hypothesis open for prospective validation.
OBJECTIVE: In humans, evidence about the association between levels of monocyte chemoattractant protein-1 (MCP-1), its coding gene chemokine (C-C motif) ligand 2 (CCL2), and risk of coronary artery disease (CAD) is contradictory. METHODS AND RESULTS: We performed a nested case-control study in the prospective EPIC-Norfolk cohort investigating the relationship between CCL2 single-nucleotide polymorphisms (SNPs), MCP-1 concentrations, and the risk of future CAD. Cases (n=1138) were apparently healthy men and women aged 45 to 79 years who developed fatal or nonfatal CAD during a mean follow-up of 6 years. Controls (n=2237) were matched by age, sex, and enrollment time. Using linear regression analysis no association between CCL2 SNPs and MCP-1 serum concentrations became apparent, nor did we find a significant association between MCP-1 serum levels and risk of future CAD. Finally, Cox regression analysis showed no significant association between CCL2 SNPs and the future CAD risk. In addition, we did not find any robust associations between the CCL2 haplotypes and MCP-1 serum concentration or future CAD risk. CONCLUSIONS: Our data do not support previous publications indicating that MCP-1 is involved in the pathogenesis of CAD.
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Wijk et al. (2010) conducted a case-control in Coronary Artery Disease (n=3,375). CCL2 single-nucleotide polymorphisms and MCP-1 serum concentrations vs. Matched controls was evaluated on Risk of future fatal or nonfatal coronary artery disease. CCL2 single-nucleotide polymorphisms and MCP-1 serum concentrations were not significantly associated with the risk of future coronary artery disease over a mean 6-year follow-up.
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