Fig. 3.
The beneficial effects of MSCs were partially dependent on the activation of the β-catenin-dependent Wnt signaling pathway. a, b Transwell culturing of MSCs with MS-1 ameliorated the H2O2-induced cell apoptosis, but the treatment of XAV-939, a Wnt/β-catenin-mediated transcription antagonist, abolished those effects partially (a shows the results of double staining of annexin V/PI flow cytometry and b shows the results of TUNEL staining). c XAV-939 also abolished the MSC-CM-induced cell viability restoration observed by MTT tests. d Confirmation of an increase in the apoptosis after XAV-939 treatment by cleaved caspase 3 western blotting analysis, and the western blotting results of the impaired endothelium function indicated by eNOS activation and expression of VCAM. Quantification of bands performed using ImageJ software. *p < 0.05, **p < 0.001. t-eNOS total endothelial nitric oxide synthase, p-eNOS phosphorylated-endothelial nitric oxide synthase, ICAM intercellular cell adhesion molecule, MSC mesenchymal stromal cell, PI propidium iodide, VCAM vascular cell adhesion molecule