GSE203523
Loss of PRMT2 in myeloid cells in normoglycemic mice phenocopies impaired regression of atherosclerosis in diabetic mice
The goal of this study is to determine whether PRMT2 plays a causal role in the impairment of atherosclerosis regression in diabetes. We examined the consequence of deleting PRMT2 in myeloid cells during the regression of atherosclerosis in normal and diabetic mice. We found significant impairment of atherosclerosis regression under normoglycemic conditions in mice lacking PRMT2 (Prmt2-/-) in myeloid cells that mimic the decrease in regression of atherosclerosis in WT mice under diabetic conditions. This was associated with increased plaque macrophage retention. PRMT2-deficient plaque CD68+ cells under normoglycemic conditions showed increased expression of genes involved in cytokine signaling and inflammation compared to WT cells by RNA seq. Thus, the loss of PRMT2 is causally linked to impaired atherosclerosis regression. Overall design: CD68+ cells were selected from atherosclerotic plaques from WT and Prmt2-/- mice undergoing regression by laser capture microdissection (LCM). Foam cells were identified under a microscope and verified by positive CD68 staining. For each animal, CD68+ cells were captured from 50–60 frozen sections. RNA was isolated and RNA -seq was performed to determine genes differentially expressed in WT and Prmt2-/-  CD68+ cells under non-diabetic conditions.