Results
| PMID | 16192641 |
| Gene Name | MMP9 |
| Condition | Endometriosis |
| Association |
Associated |
| Sex | Female |
| Associated genes | MMP-9,PGE(2) |
| Other associated phenotypes |
Endometriosis |
|
Am J Pathol. 2005 Oct;167(4):1061-9. Wu, Meng-Hsing| Shoji, Yutaka| Wu, Meng-Chi| Chuang, Pei-Chin| Lin, Chen-Chung| Huang, Mei-Feng| Tsai, Shaw-Jenq Department of Obstetrics and Gynecology, National Cheng Kung University Medical College, Tainan, Taiwan, Republic of China. Decreased phagocytotic ability of macrophages has been reported to be associated with the severity of endometriosis, although the underlying mechanism remains uncharacterized. Expression and secretion of matrix metalloproteinase (MMP)-9 by macrophages is a means to degrade the extracellular matrix of cells that are designated for phagocytosis. Here, we describe the regulation of MMP-9 expression and activity in peritoneal macrophages of women with endometriosis. Results demonstrated that peritoneal macrophages isolated from women with endometriosis have decreased levels of protein and enzyme activity of MMP-9. Treatment of macrophages with peritoneal fluid obtained from patients with severe endometriosis inhibited MMP-9 expression and gelatinase activity. Further investigation identified prostaglandin (PG) E(2) as the major factor in the peritoneal fluid that inhibited MMP-9 activity. The inhibitory effect of PGE(2) was mediated via the EP2/EP4-dependent PKA pathway. Furthermore, expression of tissue inhibitor of metalloproteinase-1, tissue inhibitor of metalloproteinase-2, and RECK in macrophages was not affected by treatment with PGE(2), indicating the effect of PGE(2) on suppressing MMP-9 activity was not mediated by up-regulation of its inhibitor. Our results suggest that decreased phagocytotic capability of peritoneal macrophage in patients with endometriosis may be caused by PGE(2)-mediated decreases in MMP-9 expression. Mesh Terms: Ascitic Fluid/chemistry| Blotting, Western| Case-Control Studies| Cells, Cultured| Dinoprostone/metabolism/*pharmacology| Endometriosis/*enzymology/pathology| Female| Gene Expression Regulation, Enzymologic/drug effects| Humans| Interferon-gamma/ |
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