Skip to main content
Fig. 7 | Cell Communication and Signaling

Fig. 7

From: Extracellular succinate derived from ectopic milieu drives adhesion and implantation growth of ectopic endometrial stromal cells via the SUCNR1 signal in endometriosis

Fig. 7

Succinate Induce the Enrichment of SUCNR1+ Macrophages and Ectopic Lesion Formation in vivo. A The wight change of mouse EMs model during the 2 weeks. Ctrl: PBS treatment; M: Model group; M + S: Model with succinate treatment group. The data are expressed as the mean ± SEM. (One-way ANOVA) *P < 0.05, **P < 0.01 and ***P < 0.001. B The macroscopic observation of the morphology of endometriosis-like lesions from endometriosis mouse models. M: Model group, M + S: Model with succinate treatment group. C-D The number and wight of EMs lesions was measured after the treatment of succinate (100 mg/kg) or PBS. M: Model group, M + S: Model with succinate treatment group. (Student’s t-test) *P < 0.05, **P < 0.01 and ***P < 0.001. E-I The levels of CD80, CD163 and SUCNR1 on peritoneal CD11b(+)F4/80(+) macrophages from mouse models were analyzed by using flow cytometry. MFI of SUCNR1 on M1 and M2 macrophages obtained were shown respectively. Ctrl: marked in red; M: marked in blue; M + S: marked in orange. (One-way ANOVA) *P < 0.05, **P < 0.01 and ***P < 0.001. J MMP9 and ICAM-1 expression in endometriosis-like lesion from model mice (M) and succinate exposing mice (M + S) by immunohistochemistry. M: Model group; M + S: Model with succinate treatment group. Original magnification: × 200

Back to article page