Results
| PMID | 27624484 |
| Gene Name | IL24 |
| Condition | Endometriosis |
| Association |
Associated |
| Sex | Female |
| Other associated phenotypes |
Endometriosis |
|
Reproduction. 2016 Dec;152(6):673-682. doi: 10.1530/REP-16-0278. Epub 2016 Sep Shao, Jun| Zhang, Bing| Yu, Jia-Jun| Wei, Chun-Yan| Zhou, Wen-Jie| Chang, Kai-Kai| Yang, Hui-Li| Jin, Li-Ping| Zhu, Xiao-Yong| Li, Ming-Qing Laboratory for Reproductive ImmunologyHospital of Obstetrics and Gynecology.| Laboratory for Reproductive ImmunologyHospital of Obstetrics and Gynecology.| Laboratory for Reproductive ImmunologyHospital of Obstetrics and Gynecology.| Laboratory for Rep Macrophages play an important role in the origin and development of endometriosis. Estrogen promoted the growth of decidual stromal cells (DSCs) by downregulating the level of interleukin (IL)-24. The aim of this study was to clarify the role and mechanism of IL-24 and its receptors in the regulation of biological functions of endometrial stromal cells (ESCs) during endometriosis. The level of IL-24 and its receptors in endometrium was measured by immunohistochemistry. In vitro analysis was used to measure the level of IL-24 and receptors and the biological behaviors of ESCs. Here, we found that the expression of IL-24 and its receptors (IL-20R1 and IL-20R2) in control endometrium was significantly higher than that in eutopic and ectopic endometrium of women with endometriosis. Recombinant human IL-24 (rhIL-24) significantly inhibited the viability of ESCs in a dosage-dependent manner. Conversely, blocking IL-24 with anti-IL-24 neutralizing antibody promoted ESCs viability. In addition, rhIL-24 could downregulate the invasiveness of ESCs in vitro After co-culture, macrophages markedly reduced the expression of IL-24 and IL-20R1 in ESCs, but not IL-22R1. Moreover, macrophages significantly restricted the inhibitory effect of IL-24 on the viability, invasion, the proliferation relative gene Ki-67, proliferating cell nuclear antigen (PCNA) and cyclooxygenase2 (COX-2), and the stimulatory effect on the tumor metastasis suppressor gene CD82 in ESCs. These results indicate that the abnormally low level of IL-24 in ESCs possibly induced by macrophages may lead to the enhancement of ESCs' proliferation and invasiveness and contribute to the development of endometriosis. Mesh Terms: Adult| *Cell Movement| Cell Proliferation| Coculture Techniques| Endometriosis/metabolism/*pathology| Endometrium/metabolism/*pathology| Female| Humans| Interleukins/*antagonists & inhibitors/metabolism| Macrophages/metabolism/*pathology| Signal |
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