Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 계명찬 | - |
dc.date.accessioned | 2018-03-07T04:32:30Z | - |
dc.date.available | 2018-03-07T04:32:30Z | - |
dc.date.issued | 2012-03 | - |
dc.identifier.citation | Endocrinology, 2012, 153(4), P.1925-1935 | en_US |
dc.identifier.issn | 0013-7227 | - |
dc.identifier.uri | https://academic.oup.com/endo/article/153/4/1925/2424051 | - |
dc.description.abstract | Oviductal disease is a primary cause of infertility, a problem that largely stems from excessive inflammation of this key reproductive organ. Our poor understanding of the mechanisms regulating oviductal inflammation restricts our ability to diagnose, treat, and/or prevent oviductal disease. Using mice, our objective was to determine the spatial localization, regulatory mechanism, and functional attributes of a hypothesized regulator of oviductal inflammation, the hematopoietic form of prostaglandin D synthase (HPGDS). Immunohistochemistry revealed specific localization of HPGDS to the oviduct's epithelium. In the isthmus, expression of HPGDS was consistent. In the ampulla, expression of HPGDS appeared dependent uponstage of the estrous cycle. HPGDS was expressed in the epithelium of immature and cycling mice but not in the oviducts of estrogen receptor alpha knockouts. Two receptor subtypes bind PGD(2): PGD(2) receptor and G protein-coupled receptor 44. Expression of mRNA for Ptgdr was higher in the epithelial cells (EPI) than in the stroma (P < 0.05), whereas mRNA for Gpr44 was higher in the stroma than epithelium (P < 0.05). Treatment of human oviductal EPI with HQL-79, an inhibitor of HPGDS, decreased cell viability (P < 0.05). Treatment of mice with HQL-79 increased mRNA for chemokine (C-C motif) ligands 3, 4, and 19; chemokine (C-X-C motif) ligands 11 and 12; IL-13 and IL-17B; and TNF receptor superfamily, member 1b (P < 0.02 for each mRNA). Overall, these results suggest that HPGDS may play a role in the regulation of inflammation and EPI health within the oviduct. (Endocrinology 153: 1925-1935, 2012) | en_US |
dc.description.sponsorship | This work was supported by Start-up funds from the University of Kentucky (P.J.B.), National Institutes of Health Grants P20 RR15592 (P.J.B., C. K., M.Jo) and K12 DA014040 (P.J.B.), and the Korean Government Grant NRF 2011-0017084 (to M.C.G.). | en_US |
dc.language.iso | en | en_US |
dc.publisher | Endocrine SOC | en_US |
dc.subject | REPRODUCTIVE TECHNOLOGY SURVEILLANCE | en_US |
dc.subject | CHLAMYDIA-TRACHOMATIS INFECTION | en_US |
dc.subject | ESTROGEN-RECEPTOR-ALPHA | en_US |
dc.subject | GENE-EXPRESSION | en_US |
dc.subject | UNITED-STATES | en_US |
dc.subject | MESSENGER-RNA | en_US |
dc.subject | DOMINANT EXPRESSION | en_US |
dc.subject | TUBAL OCCLUSION | en_US |
dc.subject | BETA-TRACE | en_US |
dc.subject | RAT-BRAIN | en_US |
dc.title | Hematopoetic Prostaglandin D Synthase: An ESR1-Dependent Oviductal Epithelial Cell Synthase | en_US |
dc.type | Article | en_US |
dc.relation.no | 4 | - |
dc.relation.volume | 153 | - |
dc.identifier.doi | 10.1210/en.2011-1900 | - |
dc.relation.page | 1925-1935 | - |
dc.relation.journal | ENDOCRINOLOGY | - |
dc.contributor.googleauthor | Bridges, Phillip J | - |
dc.contributor.googleauthor | Jeoung, Myoungkun | - |
dc.contributor.googleauthor | Sapsford, Lindsay A. | - |
dc.contributor.googleauthor | Trudgen, Kourtney | - |
dc.contributor.googleauthor | Ko, Chemyong | - |
dc.contributor.googleauthor | Park, Ji Yeon | - |
dc.contributor.googleauthor | Jo, Misung | - |
dc.contributor.googleauthor | Shim, Sarah | - |
dc.contributor.googleauthor | Lee, Jae Eun | - |
dc.contributor.googleauthor | Gye, Myung Chan | - |
dc.relation.code | 2012202819 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF NATURAL SCIENCES[S] | - |
dc.sector.department | DEPARTMENT OF LIFE SCIENCE | - |
dc.identifier.pid | mcgye | - |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.