1995 Fiscal Year Final Research Report Summary
Expression and control mechanisms of prostaglandin H2 synthase in endometrium and decidua
| Project/Area Number |
05671396
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Saitama Medical School |
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Principal Investigator |
ISHIHARA Osamu Lecturer, Dep.of Obstetrics & Gynaecology, Saitama Medical Center, Saitama Medical School, 医学部, 講師 (70176212)
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| Co-Investigator(Kenkyū-buntansha) |
IINO Yoshiaki Saitama Medical Center, Saitama Medical School, 医学部, 助手 (20211021)
SAITOH Mashiro Saitama Medical Center, Saitama Medical School, 医学部, 助手 (50225736)
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| Project Period (FY) |
1993 – 1995
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| Keywords | Cyclooxygenase / Decidua / Interleukin-1 / NS-398 / Progesterone / Dexamethasone |
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| Research Abstract |
In order to clarify the involvement of two types of cyclooxygenase (COX) in decidual PG production, subsequent study was undertaken by using in vitro decidual stromal cells culture system.
Immunocytochemical study with specific antibody revealed the presence of COX-2 as well as COX-1 in decidual stromal cells obtained at the time of therapeutic abortion between 6 to 8 weeks. In contrast to COX-1 which was apparently expressed constitutively, COX-2 was induced by the addition of interleukin-1 (IL-1) in the absence of serum in culture medium. The basal staining level of COX-2 was significantly lower than that of COX-1. The addition of dexamethasone of progesterone attenuated the induction of COX-2 in terms of both enzyme staining and PGE2 production, which implied the possible involvement of progesterone in the inhibitory mechanism of prostaglandin synthesis by decidua in early pregnancy. In addition, a specific inhibitor of COX-2, NS-398, dose dependently inhibited the PGE2 production by decidual cells stimulated with IL-1 and completely blocked PG production at the dose of 10^<-6>M.
These results suggest that PG production by dedidual stromal cells from early pregnancy wholely depend upon COX-2 pathway in this in vitro culture condition and it seems likely that COX-1 activity may be under control of different mechanism such as arachidonic acid availability or previously reported enzyme inhibitory protein.
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