Fig. 7
The therapeutic effect of PMV-delivered CTGF was mediated by ERK1/2-STAT3 axis. A The expression and the phosphorylation level of STAT3 in LPS-stimulated VECs treated by modified PMVs with or without ERK1/2 agonist (n = 3). B Laser confocal microscopy analysis of p-STAT3 (green) in LPS-stimulated VECs treated by modified PMVs with or without ERK1/2 agonist (n = 5, bar = 40 μm). C Scratch experiment of LPS-stimulated VECs treated by ERK1/2 inhibitor with or without STAT3 agonist, the representative images are shown (n = 5, bar = 100 μm). D CCK8 proliferation of LPS-stimulated VECs treated by ERK1/2 inhibitor with or without STAT3 agonist (n = 6). E Tube formation of LPS-stimulated VECs treated by ERK1/2 inhibitor with or without STAT3 agonist, the representative images are shown (n = 5, bar = 50 μm). F Statistical analysis of the tube length in E (n = 5). Ctl: normal group; LPS: LPS group; PMV: PMV-treated LPS group; PMVCTGF−down: CTGF-downregulated PMV + LPS group. ERK-ago: ERK1/2 agonist Senkyunolide I. ERK-ihi: EKR1/2 inhibitor SCH772984. STAT3-ago: STAT3 agonist UVB. ***P < 0.001, **P < 0.01