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Fig. 2 | Stem Cell Research & Therapy

Fig. 2

From: Glutamate regulates gliosis of BMSCs to promote ENS regeneration through α-KG and H3K9/H3K27 demethylation

Fig. 2

α-KG increases the expression of characteristic glial cell proteins and demethylation of BMSCs; succinate inhibits the expression of characteristic glial cell proteins and demethylation of BMSCs. DM-α-KG (4 mM) or DM-succinate (4 mM) were incubated with BMSCs for 24 h. A and B Representative immunoblot bands and histogram of relative expression for the GFAP (Control:1, α-KG: 1.42 ± 0.09, Suc:0.68 ± 0.15), S100B (Control:1, α-KG: 1.61 ± 0.13, Suc:0.34 ± 0.11), and GDNF (Control:1, α-KG: 1.31 ± 0.08, Suc:0.73 ± 0.12) proteins. GAPDH was used as a loading control. C and D Representative immunoblot bands and histogram of relative expression for the H3K9me3(Control:1, α-KG: 0.15 ± 0.02, Suc:1.42 ± 0.11), H3K9me1(Control:1, α-KG: 1.36 ± 0.05, Suc:0.61 ± 0.05), H3K27me3 (Control:1, α-KG: 0.27 ± 0.06, Suc:1.3 ± 0.13), and H3K27me1 (Control:1, α-KG: 1.45 ± 0.23, Suc:0.63 ± 0.09) proteins. H3 was used as a loading control. EH Representative immunofluorescence images for H3K9me3 (red), H3K9me1 (red), H3K27me3 (green), and H3K27me1 (green) of BMSCs in each group, the nuclei were labeled with DAPI (blue). Con: control; α-KG: alpha-ketoglutarate; Suc: succinate. These results are representative of at least three times independent experiments. *P < 0.05, **P < 0.01

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