Results
| PMID | 24133578 |
| Gene Name | IL22 |
| Condition | Endometriosis |
| Association |
Associated |
| Sex | Female |
| Associated genes | IL-22, IL-22R1, IL-10R2) |
| Other associated phenotypes |
Endometriosis |
|
Int J Clin Exp Pathol. 2013 Sep 15;6(10):2011-20. eCollection 2013. Guo, Yan| Chen, Ying| Liu, Li-Bing| Chang, Kai-Kai| Li, Hui| Li, Ming-Qing| Shao, Jun Department of Pathology, Yixing Second People's Hospital Yixing, Jiangsu Province 214221, People's Republic of China. 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. Mesh Terms: Cell Proliferation/*drug effects| Chemokine CCL2/*metabolism| Dose-Response Relationship, Drug| Endometriosis/metabolism/pathology| Endometrium/drug effects/*metabolism/pathology| Female| Humans| Interleukin-8/*metabolism| Interleukins/*metabolism |
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