Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9943241 | The American Journal of Pathology | 2005 | 9 Pages |
Abstract
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) E2 as the major factor in the peritoneal fluid that inhibited MMP-9 activity. The inhibitory effect of PGE2 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 PGE2, indicating the effect of PGE2 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 PGE2-mediated decreases in MMP-9 expression.
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Authors
Meng-Hsing Wu, Yutaka Shoji, Meng-Chi Wu, Pei-Chin Chuang, Chen-Chung Lin, Mei-Feng Huang, Shaw-Jenq Tsai,