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CCL18 promotes endometriosis by increasing endometrial cell migration and neuroangiogenesis

Authors

Yangying Peng
pengyy20220329@163.com
https://orcid.org/0000-0003-3280-3820
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, China.
Shaojie Ding
Department of Obstetrics and Gynecology, Women’s Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Ping Xu
Department of Obstetrics and Gynecology, Women’s Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Xueyan Zhang
Department of Obstetrics and Gynecology, Women’s Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Jianzhang Wang
Department of Obstetrics and Gynecology, Women’s Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Tiantian Li
Assisted Reproduction Unit, Department of Obstetrics and Gynecology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Liyun Liao
Xiangshan First People’s Hospital Medical and Health Group, Ningbo, China.
Xinmei Zhang
https://orcid.org/0000-0001-7122-6435
Department of Obstetrics and Gynecology, Women’s Hospital, Zhejiang University School of Medicine, Hangzhou, China.

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.

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Ethics Approval

the experimental protocols were approved by the Ethics Committee of the Women’s Hospital, Zhejiang University School of Medicine., The treatment of the mice in this study was approved by the Ethics Committee of Animal Laboratory, Zhejiang University

Supporting Agencies

Natural Science Foundation of Zhejiang Province, National Natural Science Foundation of China

How to Cite

Peng, Y., Ding, S., Xu, P., Zhang, X., Wang, J., Li, T., … Zhang, X. (2024). CCL18 promotes endometriosis by increasing endometrial cell migration and neuroangiogenesis. European Journal of Histochemistry, 68(3). https://doi.org/10.4081/ejh.2024.4052
Copyright (c) 2024 The Author(s) Creative Commons License

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