Results
| PMID | 27987338 |
| Gene Name | IL1B |
| Condition | Endometriosis |
| Association |
Associated |
| Sex | Female |
| Associated genes | IL4, VCL |
| Other associated phenotypes |
Endometriosis |
|
J Obstet Gynaecol Res. 2017 Feb;43(2):308-319. doi: 10.1111/jog.13201. Epub 2016 Wu, Rong-Feng| Yang, Hui-Ming| Zhou, Wei-Dong| Zhang, Li-Rong| Bai, Jian-Bing| Lin, Dian-Chao| Ng, Tai-Wei| Dai, Song-Juan| Chen, Qiong-Hua| Chen, Qing-Xi State Key Laboratory of Cellular Stress Biology and Key Laboratory of the Ministry of Education for Coastal and Wetland Ecosystems, School of Life Sciences, Xiamen University, Xiamen, China.| State Key Laboratory of Cellular Stress Biology and Key Labo AIM: Lipoxin A4 (LXA4 ) can function as an endogenous 'breaking signal' in inflammation and plays an important role in the progression of endometriosis. The proteome responses to interleukin-1beta (IL-1beta) or LXA4 in human endometriotic stromal cells (ESC) are not well understood. METHODS: In this study, primary ESC were cultured from ovarian endometriosis tissue. Three groups were established: the control group; the IL-1beta stimulation group; and the IL-1beta and LXA4 incubation group. Proteins were assessed on 2-D polyacrylamide gel electrophoresis (2D-PAGE), and differentially expressed protein spots were further identified on matrix-assisted laser desorption/ionization-time of flight (MALDI-TOF) mass spectrometry (MALDI-TOF-MS). Wound healing and transwell assays were performed to assess the migration and invasion of ESC after treatment. RESULTS: In total, 40 differentially expressed protein spots were identified successfully on MALDI-TOF-MS. The proteins identified were related to cell structure, metabolism, signal transduction, protein synthesis and membrane structure, processes that may be involved in the development of endometriosis. Vinculin and IL-4 were further analyzed on western blot and quantitative real-time polymerase chain reaction. Moreover, LXA4 could suppress the migration and invasion of ESC induced by IL-1beta. CONCLUSION: LXA4 may inhibit the progression of endometriosis partly by lowering or raising the effect of IL-1beta, mediated via some inflammation-related proteins (e.g. vinculin) and immune response-related protein (e.g. IL-4) in vitro. Mesh Terms: Adult| Anti-Inflammatory Agents, Non-Steroidal/*pharmacology| Endometriosis/drug therapy/*metabolism| Endometrium/cytology/drug effects/*metabolism| Female| Humans| Interleukin-1beta/drug effects/*metabolism| Lipoxins/*pharmacology| Proteomics/*me |
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