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. Author manuscript; available in PMC: 2016 Apr 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2015 Jan 22;35(4):817–828. doi: 10.1161/ATVBAHA.114.305218

Figure 6. Myocardin inhibits accumulation of macrophages in the neointima.

Figure 6

(A) Hematoxylin and eosin (H&E) and confocal images of carotid arteries from mice transduced with adenoviral vectors expressing beta-galactosidase (Ad.LacZ) control or Ad.Myocd. Carotid sections were labelled with antibodies directed against smooth muscle α-actin (ACTA2; green) and lysosome-associated membrane protein 2 (LAMP2; red). 4′,6-diamidino-2-phenylindole (DAPI; blue) counterstaining indicates nuclei. Scale bar, 100 μm. (B) Quantification of macrophages (cells positive for LAMP2) in the neointimal layers. Data are presented as mean±s.e.m. *P<0.05 Student’s t-test. Ad.LacZ (n=12) and Ad.Myocd (n=13). (C) Schematic illustrating a proposed model whereby reduced myocardin expression in contractile medial vascular smooth muscle cells (VSMCs) is a necessary permissive step in VSMC inflammatory activation following exposure to atherogenic stimuli, leading to increased leukocyte infiltration and progression of atherosclerosis. Dashed arrow represents VSMC-independent routes of disease progression.