Figure 2.

Exosomes from ADSCs Promoted EPC Migration and Tube Formation, and Upregulation of CXCR7 Helped AMI-EPCs Restore Cell Migration and Tube Formation

(A and B) EPCs from healthy controls (control-EPCs) were transfected with interfering plasmid or lentiviral interfering CXCR7 plasmid, while EPCs from acute myocardial infarction (AMI) patients (AMI-EPCs) were transfected with lentiviral plasmid or lentiviral overexpression of the CXCR7 plasmid, and cultured for 48 h. (A) Expression of CXCR7 was detected by western blotting. (B) The western blot results were normalized to β-actin. ∗∗p < 0.01, compared to the non-transfected cells of control- or AMI-EPCs. (C) Cell migration was measured using Transwell assays. The upper chamber contained EPCs; the lower chamber contained DMEM containing 10% FBS or ADSCs with or without pretreatment with 2.5 μM GW4869 for 8 h. Scale bars, 100 μm. (D) Migrated cells were calculated. ∗p < 0.05, compared to the DMEM control group; ^#p < 0.05, compared to the ADSC-treated group. (E and F) The indicated EPCs treated with supernatants of ADSCs with or without pretreatment with GW4869. (E) The tube formation assay. Scale bars, 100 μm. (F) The tube lengths were measured. The control-EPCs transfected with siRNA were normalized to 1. ∗p < 0.05, compared to the untreated group; ^#p < 0.05, compared to the ADSCs-supernatant-treated group.