L-22 enhances the invasiveness of endometrial stromal cells of adenomyosis in an autocrine manner.

Wang Q, Qing Wang, Li Wang, Wang L, Jun Shao, Yan Wang, Wang Y, Liping Jin, Jin LP, Li-Ping Jin, Li DJ, Da-Jin Li, Da‐Jin Li, Ming‐Qing Li, Li MQ, Ming-Qing Li
International journal of clinical and experimental pathology · 2014 · vol. 7(9) , pp. 5762–71 · PMID:25337217 · PMC4203188 · W2340049947
article OA: green CC0 ⤵ 14 in-corpus citations
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Adenomyosis endometrial stromal cells show increased IL-22 and its receptor expression, and IL-22 promotes their invasiveness via an autocrine mechanism.

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Abstract

It has reported that interleukin-22 (IL-22) promotes the invasion of tumor cells. IL-22 in the endometriotic milieu stimulates the proliferation of human endometrial stromal cells (ESCs). The present study aimed to elucidate whether and how IL-22 regulates the invasion of ESCs from adenomyosis. The expression of IL-22 and its receptors in normal endometrium, eutopic endometrium and ectopic lesion was analyzed by immunohistochemistry; the invasiveness of ESCs in vitro was verified by Matrigel invasion assay; and the effects of IL-22 on the correspondent functional molecules were investigated by ELISA and flow cytometry. Here we found that IL-22 and its receptors IL-22R1 and IL-10R2 in eutopic endometrium and ectopic lesion of adenomyosis were significantly higher than that of normal endometrium. Recombinant human IL-22 (rhIL-22) increased IL-22R1 and IL-10R2 levels on ESCs. Moreover, rhIL-22 promoted the invasiveness of ESCs, and inhibited the expression of metastasis suppressor gene CD82, stimulated the secretion of IL-8, RANTES, IL-6 and VEGF of ESCs. On the contrary, the neutralizing antibody for IL-22 reversed these effects. Our current study has demonstrated that IL-22 has a positive feedback on the expression of its receptors IL-22R1 and IL-10R2 on ESCs. This autocrine effect of IL-22 promotes the invasion of ESCs possibly through regulating invasion-related molecules, suggesting that the abnormal high expression of IL-22 may play an important role in ESCs invasion and finally contribute to the origin and development of adenomyosis.

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Condition tags

adenomyosis

MeSH descriptors

Adenomyosis Autocrine Communication Cell Movement Endometrium Interleukins Stromal Cells Adenomyosis Adenomyosis Case-Control Studies Cells, Cultured Chemokine CCL5 Chemokine CCL5 Endometrium Endometrium Female Humans Interleukin-22 Interleukin-6 Interleukin-6 Interleukin-8

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