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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 2. Myocardin haploinsufficiency potentiates infiltration of macrophages and inflammation during atherosclerotic lesion development.

Figure 2

Figure 2

Figure 2

(A) Confocal images of aortic root from high-fat fed ApoE−/− .Myocd+/+ (wild type, WT) and ApoE−/−. Myocd+/− (Myocd+/−) mice 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 plaque regions of the aortic root from WT (n=5) and Myocd+/− (n=5) mice fed on high-fat diet for 8 weeks. (C) Levels of serum monocyte chemotactic protein-1 (CCL2) in WT and Myocd+/− mice fed on high-fat diet for 4 weeks. Data are presented as a mean fold change relative to week 0. (D) Expression of inflammatory marker mRNA in mouse aortic root, after 1 week high fat diet. (E–H) mRNA expression of interleukin-6 (Il-6; E), Ccl2 (F), Cebpb (G) and Cebpd (H) in VSMCs derived from WT and Myocd+/− aortas after 4 hr stimulation with interleukin-1beta (IL-1B; n=3). Data are presented as mean±s.e.m. *P<0.05, ** P<0.01 and ***P<0.001 Student’s t-test.