Fig. 2: Induction of VEGF expression in rat lung epithelial L2 cells by the VEGF from MSC-derived extracellular vesicles (EVs) rescues oxidative injury in vitro.

a The VEGF levels were measured in the EVs derived from naive mesenchymal stem cells (MSCs), the EVs from scramble siRNA-transfected MSCs, the EVs from VEGF siRNA-transfected MSCs, and the EVs from fibroblasts. The EVs from VEGF siRNA-transfected MSCs or fibroblasts presented with substantially decreased VEGF levels compared to the levels in EVs from naive MSCs or scramble siRNA-transfected MSCs. Rat lung epithelial (L2) cells were treated with H₂O₂ for 1 h to induce oxidative stress. L2 cells were co-treated with naive MSCs, EVs from naive MSCs, EVs from scramble siRNA-transfected MSCs, EVs from VEGF siRNA-transfected MSCs, or EVs from fibroblasts. In the culture medium, the expression of human VEGF protein (b), human VEGF mRNA (c), rat VEGF protein (d), and rat VEGF mRNA (e) was measured. f The cell survival rate in each group was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays. The in vitro L2 cell culture groups are as follows: a, normoxic control; b, H₂O₂ control; c, H₂O₂ + human MSCs; d, H₂O₂ + EVs from human MSCs; e, H₂O₂ + EVs from scramble siRNA-transfected human MSCs; f, H₂O₂ + EVs from VEGF siRNA-transfected human MSCs; and g, H₂O₂ + EVs from human fibroblast (MRC5). Data are presented as the means ± SEM. *P < 0.05 compared to the normoxic control, ^†P < 0.05 compared to the H₂O₂ control, ^‡P < 0.05 compared to H₂O₂ + human MSCs, ^§P < 0.05 compared to H₂O₂ + EVs from human MSCs