| Inhibition of CD36-dependent phagocytosis by prostaglandin E2 contributes to the development of endometriosis. | |
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MedLine Citation:
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PMID: 20035060 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Dysfunction in macrophage-mediated phagocytosis of aberrant cells that undergo retrograde transport to the peritoneal cavity is considered an important factor in the development of endometriosis. However, the mechanisms responsible for the loss of function of macrophages remain largely unknown. Herein, we report that prostaglandin (PG) E(2), via the EP2 receptor-dependent signaling pathway, inhibits the expression of CD36 in peritoneal macrophages, resulting in reduced phagocytic ability. PGE(2)-mediated inhibition of macrophage phagocytic capability was restored by ectopic expression of CD36. Treatment with PGE(2) inhibited CD36-dependent phagocytosis of peritoneal macrophages and increased the number and size of endometriotic lesions in mice. In contrast, blockade of PGE(2) production by cyclooxygenase inhibitors enhanced the phagocytic ability of peritoneal macrophages and reduced endometriotic lesion formation. Taken together, our findings reveal a potential mechanism of immune dysfunction during endometriosis development and may contribute to the design of an effective prevention/treatment regimen. |
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Authors:
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Pei-Chin Chuang; Yiu-Juian Lin; Meng-Hsing Wu; Lih-Yuh C Wing; Yutaka Shoji; Shaw-Jenq Tsai |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2009-12-24 |
Journal Detail:
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Title: The American journal of pathology Volume: 176 ISSN: 1525-2191 ISO Abbreviation: Am. J. Pathol. Publication Date: 2010 Feb |
Date Detail:
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Created Date: 2010-01-26 Completed Date: 2010-03-16 Revised Date: 2011-07-22 |
Medline Journal Info:
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Nlm Unique ID: 0370502 Medline TA: Am J Pathol Country: United States |
Other Details:
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Languages: eng Pagination: 850-60 Citation Subset: AIM; IM |
Affiliation:
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Department of Physiology, National Cheng Kung University Medical College, Tainan 701, Taiwan, Republic of China. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antigens, CD36 / genetics, metabolism, physiology* Cells, Cultured Dinoprostone / pharmacology, physiology* Down-Regulation / drug effects Endometriosis / chemically induced, etiology*, genetics, metabolism Female Gene Expression Regulation / drug effects Humans Macrophages, Peritoneal / drug effects, metabolism, pathology Mice Mice, Inbred C57BL Peritoneal Diseases / chemically induced, etiology*, genetics, metabolism Phagocytosis* / drug effects, genetics, physiology Receptors, Prostaglandin E / genetics, metabolism, physiology Receptors, Prostaglandin E, EP2 Subtype U937 Cells |
| Chemical | |
Reg. No./Substance:
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0/Antigens, CD36; 0/PTGER2 protein, human; 0/Ptger2 protein, mouse; 0/Receptors, Prostaglandin E; 0/Receptors, Prostaglandin E, EP2 Subtype; 363-24-6/Dinoprostone |
| Comments/Corrections | |
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