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Growth-differentiation factor 15 (GDF-15) is expressed in low to moderate levels in most healthy tissues and increases in response to inflammation. GDF-15 is associated with cardiovascular dysfunction and over-expressed in the myocardium of patients with myocardial infarction (MI). However, little is known about the function of GDF-15 in cardiovascular disease, and the underlying regulatory network of GDF-15 is not known. To investigate a possible association between GDF-15 levels and DNA methylation, we performed a genome-wide DNA methylation study of white blood cells in a population-based study ( N  = 717). Significant loci where replicated in an independent cohort ( N  = 963). We also performed a gene ontology (GO) enrichment analysis. We identified and replicated 16 CpG-sites (false discovery rate [FDR] &lt; 0.05), at 11 independent loci including  MIR21. MIR21  encodes a microRNA (miR-21) that has previously been shown to be associated with the development of heart disease. Interestingly,  GDF15  mRNA contains a binding site for miR-21. Four sites were also differentially methylated in blood from participants previously diagnosed with MI and 14 enriched GO terms (FDR &lt; 0.05, enrichment &gt; 2) were identified, including ‘cardiac muscle cell differentiation’. This study shows that GDF-15 levels are associated with differences in DNA methylation in blood cells, and a subset of the loci are also differentially methylated in participants with MI. However, there might be interactions between GDF-15 levels and methylation in other tissues not addressed in this study. These results provide novel links between GDF-15 and cardiovascular disease.

Genome-wide DNA methylation study identifies genes associated with the cardiovascular biomarker GDF-15