Chemokine ligand 2 genetic variants, serum monocyte chemoattractant protein-1 levels, and the risk of coronary artery disease.
Arteriosclerosis, thrombosis, and vascular biology 2010 ; 30: 1460-6.
van Wijk DF, van Leuven SI, Sandhu MS, Tanck MW, Hutten BA, Wareham NJ, Kastelein JJ, Stroes ES, Khaw KT, and Boekholdt SM
DOI : 10.1161/ATVBAHA.110.205526
PubMed ID : 20431065
PMCID : PMC4210837
URL : https://pubmed.ncbi.nlm.nih.gov/20431065/
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.
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.
Our data do not support previous publications indicating that MCP-1 is involved in the pathogenesis of CAD.