Autor: |
Peng Y; Department of Obstetrics and Gynecology, Women's Hospital, Zhejiang University School of Medicine, Hangzhou; Department of Obstetrics and Gynecology, Huangyan Hospital of Wenzhou Medical University, Taizhou First People's Hospital, Taizhou. pengyy20220329@163.com., Ding S; Department of Obstetrics and Gynecology, Women's Hospital, Zhejiang University School of Medicine, Hangzhou. dsjd12345@zju.edu.cn., Xu P; Department of Obstetrics and Gynecology, Women's Hospital, Zhejiang University School of Medicine, Hangzhou. xuping330103@zju.edu.cn., Zhang X; Department of Obstetrics and Gynecology, Women's Hospital, Zhejiang University School of Medicine, Hangzhou. 5318022@zju.edu.cn., Wang J; Department of Obstetrics and Gynecology, Women's Hospital, Zhejiang University School of Medicine, Hangzhou. jianzhang.wang@zju.edu.cn., Li T; Assisted Reproduction Unit, Department of Obstetrics and Gynecology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou. 11718248@zju.edu.cn., Liao L; Xiangshan First People's Hospital Medical and Health Group, Ningbo. mujianying@live.cn., Zhang X; Department of Obstetrics and Gynecology, Women's Hospital, Zhejiang University School of Medicine, Hangzhou. zhangxinm@zju.edu.cn. |
Abstrakt: |
Endometriosis is an estrogen-dependent inflammatory gynecological disease whose pathogenesis is unclear. C-C motif chemokine ligand 18 (CCL18), a chemokine, is involved in several inflammatory diseases. In this study, we aimed to investigate the role of CCL18 in endometriosis and its underlying mechanisms. Human endometrium and peritoneal fluid were obtained from women with and without endometriosis for molecular studies. The expression level of CCL18 in each tissue sample was examined by RNA sequencing analysis, quantitative PCR analysis and immunohistochemistry staining. The effects of CCL18 on cell migration, tube formation and neurite growth were investigated in vitro using primary endometrial cells, human umbilical vein endothelial cells (HUVECs) and dorsal root ganglion (DRG) neurons, respectively. Moreover, the development of endometriosis in mice was studied in vivo by blocking CCL18. CCL18 was shown to be overexpressed in endometrial foci and peritoneal fluid in women with endometriosis and was positively correlated with endometriosis pain. In vitro, CCL18 promoted the migration of ectopic endometrial cells, tube formation of HUVECs, and nerve outgrowth of DRG neurons. More importantly, inhibition of CCL18 significantly suppressed lesion development, angiogenesis, and nerve infiltration in a mouse model of endometriosis. In conclusion, CCL18 may play a role in the progression of endometriosis by increasing endometrial cell migration and promoting neuroangiogenesis. |