FoxC1-Induced Vascular Niche Improves Survival and Myocardial Repair of Mesenchymal Stem Cells in Infarcted Hearts

Figure 7

Overexpression of FoxC1 reduced MSC differentiation into myofibroblasts and macrophages in the IHs. (a–c) The expression of macrophage and myofibroblast markers in the EGFP-positive (EGFP⁺) cells was examined by FACS. (a) Three images represented representative phenotypes of gated EGFP⁺ in total cardiomyocytes, α-SMA⁺collagen I⁺, or CD80/CD11b cells evaluated by FACS in transplanted MSCs. (b, c) The graphical images represent the statistical results of FACS. (d) Equal protein loading was assessed by immunoblotting for myofibroblast marker proteins, including α-SMA, collagen I, and macrophage marker proteins, CD80 and CD11b, in transplanted MSCs. (e) Quantitative analysis of α-SMA, collagen I, CD80, and CD11b protein expression in IHs treated with MSCs in the presence or absence of the adFoxC1 or siFoxC1. All graphical data are the . vs. the MSCs engrafted into the CON IHs and ^† vs. the MSCs engrafted into the adFoxC1 IHs ( per group). (f–i) Representative images of immunofluorescence staining for α-SMA (f, red), collagen I (g, red), CD80 (h, red), or CD11b (i, red) in EGFP- (green) prelabeled MSCs engrafted as mentioned previously. Nuclei were stained with DAPI (blue). . Note that FoxC1 overexpression strongly reduced the expression of myofibroblast markers and macrophage markers in the adFoxC1 group, whereas significant increases in the levels of these proteins were observed in the siFoxC1 group (arrows).