CCL 19/ CCR 7 contributes to the pathogenesis of endometriosis via PI 3K/Akt pathway by regulating the proliferation and invasion of ESC s

Problem The level of CCL 19 increased in the peritoneal fluid of women with endometriosis, but the precise mechanism of CCL 19/ CCR 7 in the pathogenesis of endometriosis remains unknown. Methods ELISA and immunohistochemistry were performed to analyze CCL 19/ CCR 7 expressions in peritoneal fluid and endometrium from women with endometriosis (n = 38) and controls (n = 32). Cell proliferation and transwell invasion assays were applied to detect proliferation and invasion of human endometrial stromal cells ( ESC s). Expressions of Bcl2, MMP 2, MMP 9, and p‐ AKT / AKT were analyzed by Western blot. Results Peritoneal fluid concentration of CCL 19 in patients with endometriosis was higher than that in controls. Those patients with moderate/severe endometriosis had significantly higher peritoneal fluid concentrations of CCL 19 compared to those with minimal/mild endometriosis. Higher CCL 19 and CCR 7 were found in the endometrium with endometriosis compared to control. CCL 19 significantly enhanced ESC proliferation and invasion through CCR 7 via activating PI 3K/Akt signal pathways. CCL 19/ CCR 7 interaction significantly enhanced phosphorylation of Akt, Bcl2, MMP 2, and MMP 9 in ESC s. Conclusion These data indicate CCL 19/ CCR 7 contributes to proliferation and invasion of ESC s, which are conducive to the pathogenesis of endometriosis through activating PI 3K/Akt pathway.