SIGNAL TRANSDUCTION IN THE DEVELOPMENT OF ENDOMETRIOSIS
| Project/Area Number |
16591643
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | THE UNIVERSITY OF TOKYO |
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Principal Investigator |
OSUGA Yutakta The University of Tokyo, Faculty of Medicine, Lecturer, 医学部附属病院, 講師 (80260496)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2005: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2004: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | endometriosis / interleukin / mitogen-activated protein kinase / proliferation / protease-activated receptor 2 / 好中球 / メカニカルストレス / ERK1 / 2 / interleukin-8 |
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| Research Abstract |
BACKGROUND : Inflammation has been proposed to play essential roles in the pathophysiology of endometriosis, in which neutrophils and mast cells have been suggested to be involved. We studied whether the protease-activated receptor 2 (PAR2), which is activated by enzymes from neutrophils and mast cells, in endometriotic stromal cells (ESC) has any implication in the development of the disease. METHODS : Cultured ESC were stimulated with various concentrations of a specific PAR2 agonist peptide. Proliferating activity of the cells was determined using immunostaining of proliferating cell nuclear antigen (a cell proliferation marker), 5-bromo-2'-deoxyuridine incorporation} into DNA and cell count. The concentrations of interleukin (IL)-6 and IL-8 were measured using specific enzyme-linked immunosorbent assay kits. The phosphorylation of three mitogen-activated protein kinases (MAPK), i.e. p38 MAPK, p42/44 MAPK and stress-activated protein Kinase/c-jun N terminal Kinase, in ESC was examined with Western blot analysis. RESULTS : Activation of PAR2 stimulated the proliferation of ESC and the secretion of IL-6 and IL-8 from ESC in a dose-dependent manner. Activation of PAR2 stimulated the phosphorylation of all three MAPK, and inhibitors of each MAPK suppressed the PAR2 activation-induced proliferation of ESC. CONCLUSIONS : The activation of PAR2 in ESC may be involved in the pathophysiology of endometriosis by inducing the growth and inflammation of endometriotic lesions.
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Report
(3 results)
Research Products
(18 results)
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[Journal Article] Mechanical, stretch upregulates IGFBP-1 secretion from decidualized endometrial stromal cells.2006
Author(s)
Harada M, Osuga Y, Takemura Y, Yoshino O, Koga K, Hirata T, Morimura C, Yano T, Yano T, Taketani Y.
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Journal Title
Am J Physiol Endocrinol Metad 290
Description
「研究成果報告書概要(欧文)」より
Related Report
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[Journal Article] GnRH II as a possible cytostatic regulator in the development of endometriosis.2005
Author(s)
Morimoto C., Osuga Y., Yano T., Takemura Y., Harada M., Hirata T., Hirota Y., Yoshino O., Koga K., Kugu K., Taketani Y
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Journal Title
Hum Reprod 20
Pages: 3212-3218
Description
「研究成果報告書概要(和文)」より
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[Journal Article] Possible involvement of thrombin/protease-activated receptor 1 system in the pathogenesis of endometriosis2005
Author(s)
Hirota Y., Osuga Y., Hirata T., Yoshino O., Koga K., Harada M., Morimoto C., Nose E., Yano T., Tsutsumi O., Taketani Y
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Journal Title
J Clin Endocrinol Metab 90
Pages: 3673-3679
Related Report
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[Journal Article] Activation, of protease-activated receptor 2 stimulates proliferation and interleukin (IL)-6 and IL-8 secretion of endometriotic stromal cells.2005
Author(s)
Hirota Y., Osuga Y., Hirata T., Harada M., Morimoto C., Yoshino O., Koga K., Yano T., Tsutsumi O., Taketani Y
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Journal Title
Hum Reprod 20
Pages: 3547-3553
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