Fig. 7

BMSCs (OE-Glud1) expressing higher glial cell characteristics markers and histone demethylation level than BMSCs (NC-Glud1) to promote ENS regeneration. A–D GFP-labeled BMSCs-NC/BMSCs-OE (green) and GFAP/S100B (red) were jointly immunostained in the transverse sections of gastric, the nuclei were labeled with DAPI (blue). E–L GFP-labeled BMSCs-NC/BMSCs-OE (green) and H3K9me1/H3K9me3/H3K27me1/H3K27me3 (red) were jointly immunostained in the transverse sections of gastric, the nuclei were labeled with DAPI (blue). M The cartoon of the mechanism that BMSCs promoting ENS regeneration. Glud1 hydrolysis metabolite glutamate affects a-KG, which further affects H3K9me3 and H3K27me3 levels and the expression of GFAP, S100B, and GDNF, which alters the BMSCs’ glial cell properties. These results are representative of at least three times independent experiments. BAC + BMSCs (NC-Glud1): BAC mice transplanted with BMSCs-NC; BAC + BMSCs (OE-Glud1): BAC mice transplanted with BMSCs-OE. ENS: enteric nervous system; Glud1: glutamate dehydrogenase 1; TCA: tricarboxylic acid; α-KG: alpha-ketoglutarate, D-2HG: D-2-hydroxyglutarate