Skip to main content
. Author manuscript; available in PMC: 2014 Jun 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2013 Apr 4;33(6):1350–1359. doi: 10.1161/ATVBAHA.112.300287

Figure 4. BMPRII expression is reduced by pro-atherogenic risk factors, while upregulated by anti-atherogenic conditions.

Figure 4

(A) ApoE−/− mice were partially ligated and fed the high-fat diet for 2 or 7 days. Frozen sections of ligated LCA exposed to d-flow were stained with PECAM-1 or BMPRII antibody (red) and representative confocal microscopy images are shown (n=6). DAPI staining of nuclei (blue) and elastic laminas (green) are shown. Arrows and * point to endothelial cells and intima leukocytes, respectively. (B) Endothelial-enriched RNAs were isolated from RCA and LCA of C57Bl6 mice at 48 h post-partial ligation, and BMPRII mRNA was determined by qPCR (n=4, *p<0.05). (C) HUVECs were exposed to static control, laminar shear (LS) or oscillatory shear (OS) in vitro for 24 h, and BMPRII expression was determined by qPCR (n=4, *p<0.05). (D) Endothelial-enriched RNAs were isolated from thoracic aortas of C57Bl6 mice, following AngII infusion for 0 to 72 h, and BMPRII was determined by qPCR (n=4, *p<0.05). (E, F) HUVECs were treated with TNFα (E) or simvastatin or rosuvastatin for 24 h (F).