Effect of interleukin-1β and lipoxin A 4 in human endometriotic stromal cells: Proteomic analysis

• Published in: The journal of obstetrics and gynaecology research 2017-02, Vol.43 (2), p.308-319
• Main Authors: 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
• Format: Article
• Language: English
• Subjects: Adult; Anti-Inflammatory Agents, Non-Steroidal - pharmacology; Endometriosis - drug therapy; Endometriosis - metabolism; Endometrium - cytology; Endometrium - drug effects; Endometrium - metabolism; Female; Humans; Interleukin-1beta - drug effects; Interleukin-1beta - metabolism; Lipoxins - pharmacology; Proteomics - methods; Stromal Cells - drug effects; Stromal Cells - metabolism
• ISSN: 1341-8076; 1447-0756
• DOI: 10.1111/jog.13201

Lipoxin A (LXA ) can function as an endogenous 'breaking signal' in inflammation and plays an important role in the progression of endometriosis. The proteome responses to interleukin-1β (IL-1β) or LXA in human endometriotic stromal cells (ESC) are not well understood. In this study, primary ESC were cultured from ovarian endometriosis tissue. Three groups were established: the control group; the IL-1β stimulation group; and the IL-1β and LXA 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. 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, LXA could suppress the migration and invasion of ESC induced by IL-1β. LXA may inhibit the progression of endometriosis partly by lowering or raising the effect of IL-1β, mediated via some inflammation-related proteins (e.g. vinculin) and immune response-related protein (e.g. IL-4) in vitro.