RNA binding motif protein 47 promotes VSMC-to-macrophage-like transition and atherosclerosis by stabilizing GALNT4 mRNA.

Vascular smooth muscle cells (VSMCs) are essential for maintaining vascular tone and participate in all stages of atherosclerosis. The transition of VSMCs into macrophage-like cells is a major source of plaque foam cells. Nevertheless, the mechanisms regulating this phenotypic transition remain elusive. RNA Binding Motif Protein 47 (RBM47) expression was increased by more than twofold in aortas of ApoE-/- mice and was markedly elevated in RBM47+α-SMA+ double-positive cells within atherosclerotic plaques. RBM47 knockdown significantly reduced plaque burden and vascular inflammation, and suppressed VSMC-to-macrophage-like transition. In POV-PC-treated VSMCs, RBM47 knockdown inhibited VSMC proliferation, migration, inflammation, and macrophage-like transition. Mechanistically, RBM47 was found to directly bind to two specific sequences within the 3'UTR of GALNT4 mRNA and enhance its stability. Functional rescue experiments confirmed that GALNT4 mediated the effects of RBM47 on VSMC-to-macrophage-like transition. These findings suggest that RBM47 contributes to atherosclerosis by stabilizing GALNT4 mRNA and promoting VSMC-to-macrophage-like transition.