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. 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 2. Loss of BMPRII induces endothelial inflammation by mechanisms dependent on ROS, NADPH oxidase, and NFκB activity.

Figure 2

(A, B) HUVECs transfected with BMPRII siRNA or Non.si were also treated with apocynin (60 μM, 2 days) or vehicle, and monocyte adhesion assay (A) or Western blot analysis (B) of cell lysates using ICAM-1 antibody were performed (mean ± SEM, n=4, *p<0.05). (C, D) Thoracic aorta sections of BMPRII+/+ApoE−/− and BMPRII+/− ApoE−/− mice were stained with dihydroethidium for ROS detection (C) or Nox1 antibody (D). Shown are representative confocal microscopy images (n=6 each). The insets show magnified views of endothelial regions. Nuclei (blue) and elastic laminas (green) are shown. L: lumen. Also shown are en face confocal images of Nox1 antibody staining (lower panels, D). (E) HUVECs were transfected with Non.si, BMPRII siRNA, BMPRII siRNA+Nox1 siRNA, or Nox1 siRNA for 2 days and analyzed by Western blots using ICAM-1, VCAM-1, BMPRII, Nox1 and β-actin antibodies. (F-H) HUVECs transfected with BMPRII siRNA or Non.si were treated with Bay11-7082 (10μM, 24 h) before monocyte adhesion assay (F), qPCR analysis for BMPRII, ICAM-1 and VCAM-1 (G), and Western blots with BMPRII, ICAM-1 and VCAM-1 antibodies (H), (n=4, *p<0.05).