Fig 1: Activation of Notch signaling is a critical mechanism for CXCR7-mediated the arterial specification by MSCs.a The transcript levels of Notch receptors, their cognate ligands, and the downstream transcription factors for ihMSCs with or without CXCR7 overexpression. b The protein levels of Notch 1, JAG1, JAG2, DLL4, and HEY1 for ihMSCs with or without CXCR7 overexpression. Data are means ± SD (n = 6). *p < 0.01 compared with control MSCs without lentiviral transduction (control). c The CBF1 reporter activities for ihMSCs with or without the SDF-1/CXCR7 axis gain-of-function for 48 h. Data are means ± SD (n = 9). *p < 0.01 compared with control MSCs without lentiviral transduction (control). d The CBF1 reporter activities for cultured in control medium, VEGF medium, VEGF medium with vehicle DMSO, and VEGF medium with CCX771 for 48 h. Data are means ± SD (n = 9). *p < 0.0001 compared with control medium. #p < 0.001 compared with VEGF medium with vehicle. e, f The transcript and protein levels of HEY1 for CXCR7-expressing MSCs and control vector-expressing MSCs (control MSCs) with or without DBZ (10 μM) treatment for 24 h. Data are means ± SD (n = 6). *p < 0.0001 compared with control MSCs. #p < 0.001 compared with vehicle treatment. g The protein levels of arterial EC markers for CXCR7-expressing MSCs and control vector-expressing MSCs (control MSCs) with or without DBZ treatment for 7 days. Data are means ± SD (n = 6). *p < 0.001 compared with control MSCs. #p < 0.01 compared with vehicle treatment. The morphology characteristics (h) and quantification of total tubes (i) and tube length (j) for in vitro tube formation of differentiating cells derived from control MSCs or CXCR7-expressing MSCs followed by treatment with DBZ for 7 days. Data are means ± SD (n = 9). *p < 0.0001 compared with control MSCs. #p < 0.0001 compared with vehicle treatment.