期刊
REPRODUCTION
卷 152, 期 6, 页码 673-682出版社
BIOSCIENTIFICA LTD
DOI: 10.1530/REP-16-0278
关键词
-
资金
- Major Research Program of the National Natural Science Foundation of China (NSFC) [91542108]
- NSFC [81471513, 81270677, 81571509]
- Shanghai Rising-Star Program [16QA1400800]
- Training Program for Young Talents of Shanghai Health System [XYQ2013104]
- Development Fund of Shanghai Talents [201557]
- Program for Zhuoxue of Fudan University
- Program for Shanghai leaders, the Program of Shanghai Outstanding Academic Leader [15XD1500900]
- Training Program for excellent academic leaders of Shanghai Health System [XBR2013093]
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.
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