Abstract
Genetics (i.e., mutations) has been assumed to be the major factor in rheumatoid arthritis (RA) etiology, but accounts for a minority of the variance in disease risk for RA. In contrast to genetics, the environment can have dramatic impacts on epigenetics that associate with disease etiology. The current study used buccal cells and purified blood monocytes from two different clinical cohorts involving Caucasian or African American female populations with or without arthritis. The differential DNA methylation regions (DMRs) between the control and RA populations were identified with an epigenome-wide association study. The DMRs (i.e., epimutations) identified in the buccal cells and monocytes were found to be distinct. The DMR associated genes were identified and many have previously been shown to be associated with arthritis. Observations demonstrate DNA methylation epimutation RA biomarkers are cell type specific and similar findings were observed with the two racial background populations. Rheumatoid arthritis susceptibility epigenetic diagnosis appears feasible and may improve the clinical management of RA and allowpreventative medicine considerations.
Highlights
Genetics has been assumed to be the major factor in rheumatoid arthritis (RA) etiology, but accounts for a minority of the variance in disease risk for RA
Females of similar age and race were collected for comparison of individuals with and without rheumatoid arthritis, Table 1
Rheumatoid arthritis impacts approximately one percent of the worldwide population, and some areas such as North America have a higher incidence of RA among the p opulation[21]
Summary
Genetics (i.e., mutations) has been assumed to be the major factor in rheumatoid arthritis (RA) etiology, but accounts for a minority of the variance in disease risk for RA. Gene associations were identified that involved a number of cellular pathways and immune related processes, such as the major histocompatibility complex (MHC), in particular the HLA-DRB1 and closely related g enes[17] These types of genetic mutation gene associations have been estimated to explain a minority of the variance in disease risk for RA18,19. Potential secondary gene associations suggest genetics can potentially explain 30% of familial disease cases[18] These GWAS and similar gene impact studies have helped to better understand the molecular basis of RA, an alternate molecular process involving epigenetics is assumed to be important and a significant factor in the etiology of RA21. An integration of environment, epigenetics and genetics is thought to be involved in the etiology and progression of rheumatoid a rthritis[21,23,24]
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