Key result
PEAR1 Factor2 DNA methylation was inversely associated with soluble P-selectin levels (Beta -0.197, p<0.0001) and white blood cell counts, linking epigenetic signatures to inflammation-dependent platelet function.
Why the study?
PEAR-1 expression is driven by DNA methylation and variants associate with platelet response and cardiovascular outcomes, but its link to platelet and leukocyte function markers required investigation.
Cohort (n=1,607)
Yes
Epigenetic signatures in the PEAR1 gene are significantly linked to inflammation-dependent platelet and leukocyte function variability.
Answers are grounded in this paper and cite their sources.
PEAR1 methylation should not yet guide therapy; hypothesis-generating for epigenetic modulation of inflammation-driven platelet function.
BACKGROUND: Platelet-endothelial aggregation receptor 1 (PEAR-1) is a transmembrane receptor involved in platelet activation and megakaryopoiesis whose expression is driven by DNA methylation. PEAR1 variants were associated with differential platelet response to activation and cardiovascular outcomes. We aimed at investigating the link between PEAR1 methylation and platelet and leukocyte function markers in a family-based population. RESULTS: We measured PEAR1 methylation in 605 Moli-family participants with available blood counts, plasma P-selectin and C-reactive protein, whole blood platelet P-selectin, and platelet-leukocyte mixed conjugate measurements. We performed principal component analysis (PCA) to identify groups of highly correlated CpG sites. We used linear mixed regression models (using age, gender, BMI, smoking, alcohol drinking, being a proband for family recruitment, being a member of myocardial infarction (MI) family as fixed effects, and family as a random effect) to evaluate associations between PEAR1 methylation and phenotypes. PEAR1 methylation Factor2, characterized by the previously identified megakaryocyte-specific CpG sites, was inversely associated with platelet-monocyte conjugates, P-selectin, and WBC counts, while positively associated with the platelet distribution width (PDW) and with leukocyte CD11b and L-selectin. Moreover, PEAR1 Factor2 methylation was negatively associated with INFLAscore, a low-grade inflammation score. The latter was partially mediated by the PEAR1 methylation effect on platelet variables. PEAR1 methylation association with WBC measurements and INFLAscore was confirmed in the independent cohort FLEMENGHO. CONCLUSIONS: We report a significant link between epigenetic signatures in a platelet functional gene and inflammation-dependent platelet function variability measured in two independent cohorts.
No takes yet. Share an insight, caveat, or question.
Izzi et al. (2019) conducted a cohort in Healthy/General Population (n=1,607). PEAR1 DNA methylation was evaluated on Association of PEAR1 Factor2 methylation with soluble P-selectin levels (Beta -0.197, p=<0.0001). PEAR1 Factor2 DNA methylation was inversely associated with soluble P-selectin levels (Beta -0.197, p<0.0001) and white blood cell counts, linking epigenetic signatures to inflammation-dependent platelet function.
Synapse has enriched 10 related papers. Consider them for comparative context: