IL-22 in the endometriotic milieu promotes the proliferation of endometrial stromal cells via stimulating the secretion of CCL2 and IL-8.

Yan Guo, Ying Chen, Libing Liu, Li-Bing Liu, Kai-Kai Chang, Kai‐Kai Chang, Hui Li, Ming-Qing Li, Ming‐Qing Li, Jun Shao
International journal of clinical and experimental pathology · 2013 · vol. 6(10) , pp. 2011–20 · PMID:24133578 · W1602040304
article OA: green CC0 ⤵ 23 in-corpus citations
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This study found that higher IL-22 levels in endometriosis stimulate endometrial stromal cell proliferation by promoting CCL2 and IL-8 secretion via STAT5, ERK1/2, and AKT pathways.

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Abstract

Interleukin-22 (IL-22) is a member of the IL-10 cytokine family and plays critical roles in inflammation, immune surveillance, and tissue homeostasis. However, whether IL-22 regulates the growth of endometrial stromal cells (ESCs), and participates in the pathogenesis of endometriosis remain unclear. In this study, we found that the expression of IL-22 and it receptors (IL-22R1 and IL-10R2) in eutopic endometrium and ectopic lesion of women with endometriosis was higher than that from healthy control. Recombinant human IL-22 (rhIL-22) stimulated the proliferation of ESCs in a dosage-dependent manner. On the contrary, anti-human IL-22 neutralizing antibody inhibited the proliferation of ESCs in vitro. The stimulatory effect of IL-22 on the proliferation of ESCs could be reversed by inhibitor of STAT5, ERK1/2 or AKT signal pathway. However, blocking STAT3, JNK or P38 signal pathway had no these effects. By Enzyme-linked immunosorbent assay (ELISA) and flow cytometry assay, we demonstrated the rhIL-22 not only stimulate the secretion of CCL2 and IL-8, but also significantly up-regulate the expression of IL-8 receptor CXCR1 on ESCs. Meanwhile, STAT5, ERK1/2 and or AKT signal inhibitors could abrogate the increase of CCL2, IL-8 and CXCR1 levels induced by rhIL-22. However, rhIL-22 had not similar influence on CCL2 receptor CCR2. Our current results suggested that the higher level of IL-22 and it receptors in eutopic endometrium may stimulate the expression of CCL2, IL-8/CXCR1, and further promote the growth of ESCs possibly through activating STAT5, MAPK/ERK1/2 and or AKT signal pathways, which may be involved in the occurrence and development of endometriosis.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Cell Proliferation Chemokine CCL2 Endometrium Interleukin-8 Interleukins Stromal Cells Cell Proliferation Chemokine CCL2 Dose-Response Relationship, Drug Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium Female Humans Interleukin-22 Interleukin-8 Interleukins

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 (39)

Cited by (23)

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