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(American Journal of Pathology. 2005;167:1061-1069.)
© 2005 American Society for Investigative Pathology

Suppression of Matrix Metalloproteinase-9 by Prostaglandin E2 in Peritoneal Macrophage Is Associated with Severity of Endometriosis

Meng-Hsing Wu*, Yutaka Shoji{dagger}, Meng-Chi Wu{dagger}, Pei-Chin Chuang{ddagger}, Chen-Chung Lin{dagger}, Mei-Feng Huang{dagger} and Shaw-Jenq Tsai{dagger}{ddagger}

From the Departments of Obstetrics and Gynecology* and Physiology{dagger} and Institute of Basic Biomedical Sciences,{ddagger} 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) 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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