Fig. 5

Succinate induces the invasion, wound healing and survival of ESCs. A Invasion assays of hESCs. Invasion assay was measured after exposure of hESC to different concentrations of succinate for 48 h, and CCL2 stimulation was used as the positive control (scale bar-200um)(n = 3). One-way ANOVA, Dunnett’s post hoc test, *P < 0.05; **P < 0.01; ***P < 0.001. B Scrath assays of hESC Scrath assay was conducted after PRE treatment in hESCs with different concentration of succinate for 48 h. Results are from 3 independent trials (n ≥ 3 for mimic) and data depicted as column mean graphs with error bars showing confidence intervals (scale bar-200um) One-way ANOVA, Dunnett’s post hoc test, *P < 0.05; **P < 0.01; ***P < 0.001. C-D Cell viability of hESCs and HMrSV5 cells was determined by CCK8 assay hESCs or HMrSV5 cells were respectively incubated with different concentrations of succinate for 24 or 48 hours. and then cell viability was determined by CCK8 assay. Data represent mean ± SEM (n = 3). *P < 0.05; **P < 0.01; ***P < 0.001. E-F Succinate does not affect the apoptosis of hESCs and HMrSV5 cells. hESCs or HMrSV5 cells were cultureed with different concentration of succinate for 48 h, and the proportion of 7AAD⁺ and Annexin V⁺ via FCM was shown in HMrSV5 cells or hESC cells via FCM(n = 3). One-way ANOVA, Dunnett’s post hoc test, *P < 0.05; **P < 0.01; ***P < 0.001