http://purl.uniprot.org/citations/25337217 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/25337217 | http://www.w3.org/2000/01/rdf-schema#comment | "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."xsd:string |
http://purl.uniprot.org/citations/25337217 | http://purl.uniprot.org/core/author | "Wang Y."xsd:string |
http://purl.uniprot.org/citations/25337217 | http://purl.uniprot.org/core/author | "Wang Q."xsd:string |
http://purl.uniprot.org/citations/25337217 | http://purl.uniprot.org/core/author | "Wang L."xsd:string |
http://purl.uniprot.org/citations/25337217 | http://purl.uniprot.org/core/author | "Shao J."xsd:string |
http://purl.uniprot.org/citations/25337217 | http://purl.uniprot.org/core/author | "Li M.Q."xsd:string |
http://purl.uniprot.org/citations/25337217 | http://purl.uniprot.org/core/author | "Li D.J."xsd:string |
http://purl.uniprot.org/citations/25337217 | http://purl.uniprot.org/core/author | "Jin L.P."xsd:string |
http://purl.uniprot.org/citations/25337217 | http://purl.uniprot.org/core/date | "2014"xsd:gYear |
http://purl.uniprot.org/citations/25337217 | http://purl.uniprot.org/core/name | "Int J Clin Exp Pathol"xsd:string |
http://purl.uniprot.org/citations/25337217 | http://purl.uniprot.org/core/pages | "5762-5771"xsd:string |
http://purl.uniprot.org/citations/25337217 | http://purl.uniprot.org/core/title | "L-22 enhances the invasiveness of endometrial stromal cells of adenomyosis in an autocrine manner."xsd:string |
http://purl.uniprot.org/citations/25337217 | http://purl.uniprot.org/core/volume | "7"xsd:string |
http://purl.uniprot.org/citations/25337217 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/25337217 |
http://purl.uniprot.org/citations/25337217 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/25337217 |
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