Effects of 17β‐estradiol on the release of monocyte chemotactic protein‐1 and MAPK activity in monocytes stimulated with peritoneal fluid from endometriosis patients

Dong-Hyung Lee, Donghyung Lee, Seung-Chul Kim, Seungchul Kim, Jong Kil Joo, Jong-Kil Joo, Jong‐Kil Joo, Hwi-Gon Kim, Hwi‐Gon Kim, Young-Jin Na, Y.J. Na, Jong‐Young Kwak, Jong-Young Kwak, Kyu Sup Lee, Kyu-Sup Lee
Journal of Obstetrics and Gynaecology Research · 2012 · vol. 38(3) , pp. 516–525 · doi:10.1111/j.1447-0756.2011.01734.x · PMID:22381103 · W1559630276
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17β-estradiol failed to suppress monocyte chemotactic protein-1 release induced by endometriosis peritoneal fluid, potentially due to altered mitogen activated protein kinase activity.

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Abstract

AIM: Hormones and inflammation have been implicated in the pathological process of endometriosis; therefore, we investigated the combined effects of 17β-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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Condition tags

endometriosis

MeSH descriptors

Ascitic Fluid Chemokine CCL2 Endometriosis Estradiol Mitogen-Activated Protein Kinases Monocytes Ovarian Diseases Ascitic Fluid Biomarkers Biomarkers Blotting, Western Chemokine CCL2 Endometriosis Enzyme-Linked Immunosorbent Assay Estradiol Female Humans In Vitro Techniques Male MAP Kinase Signaling System

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