Figure 7.
Differences in immune and angiogenic response between UC-MSCs and adult-MSCs
(A) Representative flow cytometry figures showing classical (CD11b+CD16−) and non-classical (CD11b+CD16+) monocytes populations in RAW 264.7 macrophages under resting (M(0)) and activated (M(Φ)) states (INFγ (150 ng/mL) + TNFα (50 ng/mL)) and following treatment with different MSC sources.
(B) Changes in population of monocytes (CD11b+CD16+/−) (top) and Macrophages (M1, CD86+; M2, CD206+) (bottom) following activation with INFγ (150 ng/mL) + TNFα (50 ng/mL) and treatment with different MSC sources.
(C) Changes in expression of CD202b (top) and CD31(PECAM1) (bottom) in MS-1 endothelial cells following activation with INFγ (150 ng/mL) + TNFα (50 ng/mL) and treatment with different MSC sources.
(D) Changes in Caspase-3/7 activity (top) and apoptosis (bottom) for HK-2 cellular injury models using LPS or hypoxia (ischemia)/normoxia (reperfusion). For all experiments, three different donors (n = 3) for each MSC source were used as replicates.
Data represents mean ± SEM. Statistical analysis was computed using one-way anova or Fisher's t-test; p∗ < 0.05, p∗∗ < 0.01 and p∗∗∗ < 0.001.”