期刊
JOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH
卷 38, 期 3, 页码 516-525出版社
WILEY
DOI: 10.1111/j.1447-0756.2011.01734.x
关键词
endometriosis; estrogen; mitogen activated protein kinase; monocyte chemotactic protein-1; monocyte
资金
- Medical Research Institute
- Pusan National University Hospital
- Ministry of Health and Welfare, Republic of Korea [A080416]
- National Research Foundation of Korea
- Korean Ministry of Education, Science and Technology [R13-2002-044-04001-0]
- Korea Health Promotion Institute [A080416] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
- National Research Foundation of Korea [R13-2002-044-04001-0] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Aim: Hormones and inflammation have been implicated in the pathological process of endometriosis; therefore, we investigated the combined effects of 17 beta-estradiol (E2) and peritoneal fluid obtained from patients with endometriosis (ePF) or a control peritoneal fluid (cPF) obtained from patients without endometriosis on the release of monocyte chemotactic protein-1 (MCP-1) by monocytes and the role of signaling pathways. Methods: Monocytes were cultured with ePF and cPF in the presence of E2; the MCP-1 levels in the supernatants were then measured by ELISA. In addition, mitogen activated protein kinase (MAPK) activation was measured by Western blotting of phosphorylated proteins. Results: E2 down-regulated MCP-1 release by lipopolysaccharide-or cPF-treated monocytes, but failed to suppress its release by ePF-treated monocytes. The release of MCP-1 by ePF-and cPF-treated monocytes was efficiently abrogated by p38 mitogen activated protein kinase (MAPK) inhibitors; however, the MCP-1 release by cPF-treated monocytes, but not by ePF-treated monocytes, was blocked by a MAPK kinase inhibitor. In addition, ePF and cPF induced the phosphorylation of extracellular stress regulated kinase (ERK) 1/2, p38 MAPK and c-Jun N-terminal kinase (JNK). E2 decreased the phosphorylation of p38 MAPK, but not ERK1/2 in ePF-treated monocytes; however, E2 decreased the phosphorylation of p38 MAPK, ERK1/2 and JNK in cPF-treated monocytes. Conclusions: The ability of E2 to modulate MCP-1 production is impaired in ePF-treated monocytes, which may be related to regulation of MAPK activity. These findings suggest that the failure of E2 to suppress ePF-treated production of MCP-1 may be involved in the pathogenesis of endometriosis.
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