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. Author manuscript; available in PMC: 2016 Mar 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2015 Jan 22;35(3):607–615. doi: 10.1161/ATVBAHA.114.305089

Figure 6. Integrin β3 KO inhibits CAC differentiation by increasing Notch signaling.

Figure 6

A and B. AVGs were collected from wild type and integrin β3 KO mice and subjected to real time RT-PCR (A), immunostaining of activated Notch, N1ICD, reveal an increase in Notch signaling in AVGs created in integrin β3−/− mice (B). C. Western blot confirmed an increase in Notch1 cleavage in AVGs from integrin β3 KO mice. D. CACs were treated with TGF-β1 revealed an increase in Notch ligand and its target (Western blot). E–G. If Notch signaling is inhibited, integrin β3-null platelets will improve CAC differentiation. Bone marrow-derived CACs were cocultured with wild type or integrin β3-null platelets plus TGF-β1 or DAPT. Markers of endothelial cells and platelets were detected by immunostaining, demonstrating that integrin β3 null platelets suppress CAC differentiation. This occurs via Notch activation (E). To inhibit Notch, CACs were infected with an adenovirus expressing soluble Jagged 1 (F) or with the DAPT (G), an increase in endothelial markers (VE-cadherin and CD31) were detected by real time RT-PCR followed inhibition of Notch, *, p<0.05, compared with control.