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. Author manuscript; available in PMC: 2013 Sep 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2012 Jul 5;32(9):2214–2222. doi: 10.1161/ATVBAHA.112.252015

Figure 3.

Figure 3

Bmper haploinsufficiency results in increased Bmp activity and expression of inflammatory adhesion molecules in the ApoE+/+ endothelium of the greater curvature (GC) and lesser curvature (LC) of the aortic arch. A, En face staining of the GC and LC in the aortic arch of Bmper+/− and Bmper+/− mice was performed using an antibody specific for phospho-Smad 1, 5, 8 (pSmad, green). Nuclei were counterstained with DAPI (blue). Arrows indicate pSmad positive nuclei. Scale bar: 10 μm. B, pSmad-positive nuclei were quantified as a percentage of all nuclei per field. *, P<0.05, compared to pSmad-positive nuclei (%) in the GC region of the same mice; #, P<0.05, compared to pSmad-positive nuclei (%) in the same region of wild-type littermates, n=3. C-F, En face staining was performed for ICAM1 (green in C) and VCAM1 (green in E) and the endothelial marker CD31 (red in C and E). Scale bar: 10 μm. D and F, the average intensity of ICAM1 (D) and VCAM1 (F) was measured as a fold change over the level of intensity in the GC of wild-type mice. *, P<0.05, compared to the relative expression level in the GC of the same mice; #, P<0.05, compared to the relative expression level in the same region of wild-type littermates, n=3.