CCL18 promotes endometriosis by increasing endometrial cell migration and neuroangiogenesis

Yangying Peng, Shaojie Ding, Ping Xu, Xueyan Zhang, Jianzhang Wang, Tiantian Li, Liyun Liao, Xinmei Zhang
European journal of histochemistry : EJH · 2024 · vol. 68(3) · doi:10.4081/ejh.2024.4052 · PMID:39105608 · W4401375458
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This study found that CCL18 is overexpressed in endometriosis, promoting endometrial cell migration and neuroangiogenesis, and its inhibition suppressed lesion development in a mouse model.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 · read from full text ⓘ

This study investigated whether C-C motif chemokine ligand 18 (CCL18) contributes to endometriosis and through which mechanisms by analyzing human endometrium and peritoneal fluid from women with and without endometriosis using RNA sequencing, quantitative PCR, and immunohistochemistry. CCL18 was overexpressed in endometrial foci and peritoneal fluid in endometriosis and was positively correlated with endometriosis pain; in vitro, CCL18 increased ectopic endometrial cell migration, endothelial tube formation, and DRG neurite growth. In a mouse endometriosis model, blocking CCL18 suppressed lesion development, angiogenesis, and nerve infiltration. The paper does not describe any limitation about sample size or effect direction beyond these methods, and mechanistic causality in humans is inferred through association and complementary in vitro/in vivo experiments. This paper is centrally about endometriosis — it identifies CCL18 as a driver of ectopic endometrial migration and neuroangiogenesis that promotes lesion progression.

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Abstract

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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CCL18 promotes endometriosis by increasing endometrial cell migration and neuroangiogenesis All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher. Accepted: 10 July 2024 Authors 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. 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 UniversitySupporting Agencies Natural Science Foundation of Zhejiang Province, National Natural Science Foundation of ChinaHow to Cite This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

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Outcome instruments

VAS-pain

Condition tags

mesh:D004715endometriosis

MeSH descriptors

Cell Movement Cell Movement Cell Movement Cell Movement Cell Movement Cell Movement Cell Movement Chemokines, CC Chemokines, CC Chemokines, CC Chemokines, CC Chemokines, CC Chemokines, CC Chemokines, CC Chemokines, CC Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis

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