Fig 2: Effect of GDF11 on the differentiation of MSCs into endothelial‐like cells was blocked by ERK inhibitor. MSCVector and MSCGDF11 were treated with inhibitors for ERK (SD5978) or for TGF‐β receptor (LY2109761) or with DMSO as a control during the differentiation of MSCs into endothelial‐like cells for 14 d. A, Representative results of flow cytometry analysis of MSCVector (Vector) and MSCGDF11 (GDF11) for their expression of CD31 and VEGFR2. B, Quantitative analysis of A (n = 3). C, Immunofluorescent staining of MSCVector and MSCGDF11 with antibody against CD31 (red) after culture with or without ERK inhibitor. Nucleus was stained with Hochest. Scale bars = 100 μm. D, Quantitative analysis of C (n = 3). CD31+ rate was obtained by dividing CD31+ cells (red) by total number of cells (blue) in a picture. E, Western blot analysis of proteins in MSCVector and MSCGDF11 in the presence of absence of inhibitors LY2109761 or SD5978during the differentiation of MSCs into endothelial‐like cells. F, Quantitative analysis of E (n = 2). Each WB was repeated for at least 2 times. G, Schematic diagram of the proposed mechanisms by which GDF11 promotes MSC differentiation into endothelial‐like cells. GDF11 interacts with TGF‐β receptor, resulting in activation of the ERK/EIF4E pathway, which enhances the expression of proteins for angiogenesis and anti‐apoptosis, and augment of EC markers during cultured with VEGFA. Data are presented as the mean ± SD. *P < 0.05; **P < 0.01 and ***P < 0.001. BCL‐2 for B‐cell lymphoma‐2 protein; BAX for Bcl2 Associated X Protein