Fig. 6

MSCs in FoxC1-mediated vascular microenvironments adopt endothelial cell fates after Oct4 overexpression. A Angiogenesis and fibrosis of MSCs subjected to transfection of adOct4, siOct4, or no intervention in the absence or presence of adFoxC1, as determined using immunoblotting with anti-factor VIII/α-SMA and collagen I/vimentin, respectively. B The histogram shows the quantification of the protein level relative to β-actin. C–F Double-positive cells in angiogenesis or fibrosis proteins were expressed as a percentage of factor VIII⁺CD31⁺ (C, D) or collagen I⁺vimentin⁺ (E, F) relative to all MSCs by FACS. G, H Direct fluorescence staining with VIII/α-SMA and collagen I/vimentin in MSCs culture system with or without transfection of adFoxC1, and counterstained with DAPI. Scale bars = 25 µm. I, J Correlation analysis of the double-positive rates of VIII/α-SMA (I) and collagen I/vimentin (J) in MSCs with the number of tubes/field in ECs. All data are the means ± SEM. p < 0.05: in ECs without adFoxC1, *versus MSCs treated with no intervention, ^†versus MSCs with adOct4, ^‡versus MSCs with siOct4; in ECs with adFoxC1, ^§versus MSCs treated with no intervention, ^‖versus MSCs with adOct4 (n = 10 per group). Welch ANOVA analyses were performed in B and D, and one-way ANOVA analysis was used in F. DAPI, 4′, 6-diamidino-2-phenylindole; FACS, fluorescent-activated cell sorting