Possible involvement of crosstalk between endometrial cells and mast cells in the development of endometriosis via CCL8/CCR1

Tiantian Li, Li T, Wang J, Jianzhang Wang, Guo X, Xinyue Guo, Qin Yu, Yu Q, Ding S, Shaojie Ding, Xinxin Xu, Xu X, Peng Y, Yangying Peng, Zhu L, Libo Zhu, Gen Zou, Xinmei Zhang, Zhang X
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2020 · vol. 129 , pp. 110476 · doi:10.1016/j.biopha.2020.110476 · PMID:32768961 · W3041282548
article OA: gold CC0 ⤵ 63 in-corpus citations
🔓 Open OA copy View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-07 ⓘ

This study found that crosstalk between endometrial and mast cells via CCL8/CCR1 promotes endometrial cell migration, endothelial cell proliferation and tube formation, and endometriosis development and angiogenesis in vivo.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

Abstract

The density and the activity of mast cells are associated with endometriosis. However, the role of mast cells on the pathogenesis of endometriosis remains unclear. Our study aims to investigate whether endometrial cells interact with mast cells and the involvement of their crosstalk in the development of endometriosis. The transwell assay was applied to investigate the effect of mast cells on the migratory ability of human primary endometrial cells. Mast cells were cocultured with endometrial epithelial and stromal cells respectively and total RNAs were isolated and subjected to mRNA sequencing. Next, the transwell assay, CCK-8, and tube formation were applied to study the role of CCL8 on the endometrial and endothelial cells in vitro. The mouse model was also established to confirm the role of CCL8 in the development and angiogenesis of endometriosis. CCL8 was up-regulated in mast cells when cocultured with endometrial cells. CCL8 was highly expressed in the ectopic endometrium and the serum of patients with endometriosis. CCL8 promoted the migratory ability of endometrial epithelial and stromal cells and increased the proliferation, migration, and tube formation of endothelial cells. CCR1, the receptor of CCL8, was over-expressed in the ectopic endometrium and colocalized with blood vessels in ovarian endometriomas. The inhibition of CCR1 suppressed the development and angiogenesis of endometriosis in vivo. The crosstalk between endometrial cells and mast cells in the development of endometriosis via CCL8/CCR1 was demonstrated, thereby providing a new treatment strategy for endometriosis.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Cell Communication Cell Communication Chemokine CCL8 Endometriosis Endometrium Endometrium Mast Cells Receptors, CCR1 Animals Case-Control Studies Cells, Cultured Chemokine CCL8 Chemokine CCL8 Coculture Techniques Disease Models, Animal Endometriosis Endometriosis Endometriosis Endometrium Endometrium

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (60)

Cited by (50)

Source provenance

europepmc
last seen: 2026-09-18T06:10:57.818014+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:21:47.975235+00:00
License: CC0 · commercial use OK