File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Oviductal microsomal epoxide hydrolase (EPHX1) reduces reactive oxygen species (ROS) level and enhances preimplantation mouse embryo development

TitleOviductal microsomal epoxide hydrolase (EPHX1) reduces reactive oxygen species (ROS) level and enhances preimplantation mouse embryo development
Authors
KeywordsDetoxification
Embryo
Embryo-containing
Environment
Female reproductive tract
In situ hybridization
Microsomal epoxide hydrolase
Ovariectomy
Oviduct
Steroid hormones
Issue Date2009
PublisherSociety for the Study of Reproduction. The Journal's web site is located at http://www.biolreprod.org/
Citation
Biology Of Reproduction, 2009, v. 81 n. 1, p. 126-132 How to Cite?
AbstractSomatic cell-embryo coculture enhances embryo development in vitro by producing embryotrophic factor(s) and/or removing harmful substances from the culture environment. Yet, the underlying molecular mechanisms on how somatic cells remove the toxicants from the culture medium remain largely unknown. By using suppression subtractive hybridization, we identified a number of mouse oviductal genes that were upregulated when developing preimplantation embryos were present in the oviduct. Epoxide hydrolase 1, microsomal (Ephx1 previously known as mEH) was one of these genes. EPHX1 detoxifies genotoxic compounds and participates in the removal of reactive oxygen species (ROS). The transcript of Ephx1 increases in the oviductal epithelium at the estrus stage and in Day 3 of pregnancy as well as in the uterus of ovariectomized mice injected with estrogen or progesterone. Human oviductal epithelial cells OE-E6/E7 express EPHX1 and improve mouse embryo development in vitro. Addition of an EPHX1 inhibitor, cyclohexene oxide (CHO) or 1,1,1-trichloropropene 2,3-oxide (TCPO), to the culture medium increased intracellular and extracellular ROS levels of OE-E6/E7 cells and suppressed the beneficial effect of the cells on embryo development; CHO and TCPO at these concentrations had no adverse effect on OE-E6/ E7 growth and embryo development in vitro. Taken together, EPHX1 in oviductal cells may enhance the development of cocultured embryos by protecting them from oxidative stress. Our result supports the notion that somatic cell coculture may enhance embryo development via removal of deleterious substances in the culture medium. © 2009 by the Society for the Study of Reproduction, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/87317
ISSN
2023 Impact Factor: 3.1
2023 SCImago Journal Rankings: 1.022
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheong, AWYen_HK
dc.contributor.authorLee, YLen_HK
dc.contributor.authorLiu, WMen_HK
dc.contributor.authorYeung, WSBen_HK
dc.contributor.authorLee, KFen_HK
dc.date.accessioned2010-09-06T09:28:07Z-
dc.date.available2010-09-06T09:28:07Z-
dc.date.issued2009en_HK
dc.identifier.citationBiology Of Reproduction, 2009, v. 81 n. 1, p. 126-132en_HK
dc.identifier.issn0006-3363en_HK
dc.identifier.urihttp://hdl.handle.net/10722/87317-
dc.description.abstractSomatic cell-embryo coculture enhances embryo development in vitro by producing embryotrophic factor(s) and/or removing harmful substances from the culture environment. Yet, the underlying molecular mechanisms on how somatic cells remove the toxicants from the culture medium remain largely unknown. By using suppression subtractive hybridization, we identified a number of mouse oviductal genes that were upregulated when developing preimplantation embryos were present in the oviduct. Epoxide hydrolase 1, microsomal (Ephx1 previously known as mEH) was one of these genes. EPHX1 detoxifies genotoxic compounds and participates in the removal of reactive oxygen species (ROS). The transcript of Ephx1 increases in the oviductal epithelium at the estrus stage and in Day 3 of pregnancy as well as in the uterus of ovariectomized mice injected with estrogen or progesterone. Human oviductal epithelial cells OE-E6/E7 express EPHX1 and improve mouse embryo development in vitro. Addition of an EPHX1 inhibitor, cyclohexene oxide (CHO) or 1,1,1-trichloropropene 2,3-oxide (TCPO), to the culture medium increased intracellular and extracellular ROS levels of OE-E6/E7 cells and suppressed the beneficial effect of the cells on embryo development; CHO and TCPO at these concentrations had no adverse effect on OE-E6/ E7 growth and embryo development in vitro. Taken together, EPHX1 in oviductal cells may enhance the development of cocultured embryos by protecting them from oxidative stress. Our result supports the notion that somatic cell coculture may enhance embryo development via removal of deleterious substances in the culture medium. © 2009 by the Society for the Study of Reproduction, Inc.en_HK
dc.languageengen_HK
dc.publisherSociety for the Study of Reproduction. The Journal's web site is located at http://www.biolreprod.org/en_HK
dc.relation.ispartofBiology of Reproductionen_HK
dc.subjectDetoxificationen_HK
dc.subjectEmbryoen_HK
dc.subjectEmbryo-containingen_HK
dc.subjectEnvironmenten_HK
dc.subjectFemale reproductive tracten_HK
dc.subjectIn situ hybridizationen_HK
dc.subjectMicrosomal epoxide hydrolaseen_HK
dc.subjectOvariectomyen_HK
dc.subjectOviducten_HK
dc.subjectSteroid hormonesen_HK
dc.titleOviductal microsomal epoxide hydrolase (EPHX1) reduces reactive oxygen species (ROS) level and enhances preimplantation mouse embryo developmenten_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0006-3363&volume=81&spage=126&epage=32&date=2009&atitle=Oviductal+Microsomal+Epoxide+Hydrolase+(EPHX1)+Reduces+Reactive+Oxygen+Species+(ROS)+Level+and+Enhances+Preimplantation+Mouse+Embryo+Development.en_HK
dc.identifier.emailLee, YL:h9316321@hku.hken_HK
dc.identifier.emailYeung, WSB:wsbyeung@hkucc.hku.hken_HK
dc.identifier.emailLee, KF:ckflee@hku.hken_HK
dc.identifier.authorityLee, YL=rp00308en_HK
dc.identifier.authorityYeung, WSB=rp00331en_HK
dc.identifier.authorityLee, KF=rp00458en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1095/biolreprod.108.071449en_HK
dc.identifier.pmid19321813-
dc.identifier.scopuseid_2-s2.0-67649642117en_HK
dc.identifier.hkuros158108en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-67649642117&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume81en_HK
dc.identifier.issue1en_HK
dc.identifier.spage126en_HK
dc.identifier.epage132en_HK
dc.identifier.isiWOS:000267412800015-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridCheong, AWY=24576433900en_HK
dc.identifier.scopusauthoridLee, YL=15033851800en_HK
dc.identifier.scopusauthoridLiu, WM=35548548500en_HK
dc.identifier.scopusauthoridYeung, WSB=7102370745en_HK
dc.identifier.scopusauthoridLee, KF=26643097500en_HK
dc.identifier.issnl0006-3363-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats