Alteration was found in the F2RL3 gene, which has been linked to blood clotting.
Scientists from the German Cancer Research Center say that they have found a previously unrecognized link between tobacco smoking and a gene known to influence the cardiovascular system. The research is published in the April issue of The American Journal of Human Genetics in a paper titled “Tobacco-Smoking-Related Differential DNA Methylation: 27K Discovery and Replication.”
One possible mechanism that has the potential for mediating the harmful effects of tobacco smoking is DNA methylation. Although previous studies have linked nicotine and smoking with altered methylation of several genes, comparison of methylation status between heavy smokers who do not have cancer and individuals who have never smoked has not been fully examined, according to the research team.
Methylation extents in peripheral-blood DNA were assessed at 27,578 sites in more than 14,000 gene promoter regions in 177 current smokers, former smokers, and those who had never smoked. The scientists, led by Lutz P. Breitling, Ph.D., used the Illumina HumanMethylation 27K BeadChip.
They discovered that a single locus called cg03636183 located in F2RL3 (coagulation factor II receptor-like 3) had genome-wide significance for lower methylation in smokers. This was similarly significant in 316 independent replication samples analyzed by mass spectrometry and the Sequenom EpiTyper.
F2RL3 has been linked with the process of blood clotting and with other cardiovascular functions. “Our results show that the gene coding for a potential drug target of cardiovascular importance features altered methylation patterns in smokers,” concludes Dr. Breitling.
“Intriguing perspectives lie in the possibility that this gene could be causally involved at a very initial stage of smoking-related cardiovascular pathology. A better understanding of its role might open up avenues for preventing the development of associated disease in subjects unable to quit smoking.”
