Chemokine CCL2 enhances survival and invasiveness of endometrial stromal cells in an autocrine manner by activating Akt and MAPK/Erk1/2 signal pathway

Ming‐Qing Li, Ming-Qing Li, Li MQ, Li HP, Hua-Ping Li, Huaping Li, Meng YH, Yu-Han Meng, Yuhan Meng, Wang XQ, Xiaoqiu Wang, Xiao-Qiu Wang, Zhu XY, Xiao-Yong Zhu, Xiao‐Yong Zhu, Jie Mei, Mei J, Da‐Jin Li, Da-Jin Li, Li DJ
Fertility and sterility · 2012 · vol. 97(4) , pp. 919–929.e1 · doi:10.1016/j.fertnstert.2011.12.049 · PMID:22265030 · W1964585044
article OA: closed CC0 ⤵ 43 in-corpus citations
🔓 Open OA copy View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-06 ⓘ

Chemokine CCL2 enhances endometrial stromal cell survival and invasiveness through autocrine activation of the Akt and MAPK/Erk1/2 signaling pathways.

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

Abstract

ObjectiveTo clarify the role and mechanism of CCL2 in regulating the biological functions of endometrial stromal cells (ESCs).DesignThe CCL2 effect on the viability, proliferation, and invasion in the eutopic ESCs from endometriosis.SettingResearch laboratories.Patient(s)Patients with endometriosis aged 23-47 years.Intervention(s)None.Main outcome measure(s)Signal transduction and downstream molecules from CCR2.Result(s)We have found that the secretion of CCL2 by the eutopic ESCs from endometriosis is higher than that of healthy ESCs without endometriosis. The CCL2 can enhance the viability, proliferation, and invasion of ESCs in a dosage and time-dependent manner. Anti-CCL2 neutralizing antibody and CCR2 antagonist can completely abolish the increase in viability, proliferation, and invasiveness of ESCs induced by CCL2. The CCL2 can increase the expression of proliferating cell nuclear antigen, survivin, and matrix metalloproteinase 2, and decrease the expression of tissue inhibitor of metalloproteinase 1 and 2, and promote the viability, proliferation and invasiveness of ESCs by activating Akt and MAPK/Erk1/2 signal pathway, but not p38 and JNK signal pathway.Conclusion(s)CCL2 might play an important role in regulating the functions of ESCs through Akt and MAPK/Erk1/2 signal pathway, and overexpression of CCL2 in ESCs and peritoneal fluid (PF) would lead to onset and development of endometriosis.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Autocrine Communication Cell Movement Cell Survival Chemokine CCL2 Endometriosis Endometrium Mitogen-Activated Protein Kinase 1 Mitogen-Activated Protein Kinase 3 Proto-Oncogene Proteins c-akt Signal Transduction Stromal Cells Adult Analysis of Variance Case-Control Studies Cell Proliferation Cells, Cultured Chemokine CCL2 Chemokine CCL2 Endometriosis Endometriosis

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 (42)

Cited by (46)

Source provenance

europepmc
last seen: 2026-09-19T06:15:14.566301+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:16:23.388809+00:00
unpaywall
last seen: 2026-09-17T06:32:46.214484+00:00
License: CC0 · commercial use OK