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Article: Preimplantation antagonism of adrenomedullin action compromises fetoplacental development and reduces litter size

TitlePreimplantation antagonism of adrenomedullin action compromises fetoplacental development and reduces litter size
Authors
KeywordsAdrenomedullin
Female infertility
Fetal development
Fetal resorption
Implantation
Issue Date2012
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/theriogenology
Citation
Theriogenology, 2012, v. 77 n. 9, p. 1846-1853 How to Cite?
AbstractConcentrations of adrenomedullin (ADM) in circulation, the uterus, and corpora lutea (CL) increase during pregnancy. We previously reported a temporal-spatial pattern of ADM level and gene expression of Adm and its receptor components, from early pregnancy through midpregnancy to late pregnancy in rats. Two earlier reports using an in vivo model of ADM antagonism demonstrated the important roles of ADM in the post-implantation period. Treatment with ADM receptor blocker hADM22-52 starting from gestation Day 8 or Day 14 resulted in fetal-placental growth restriction and reduction in litter size. In this study, the endogenous ADM actions were abolished in the preimplantation period by infusing the antagonist for the ADM receptor (hADM22-52) with the osmotic (Alzet) pump from Days 1-4 of pregnancy. We inferred that ADM, acting through the ADM receptor, had critical roles during preimplantation, as brief inhibition of ADM action by hADM22-52 during this period reduced litter size by restricting placental growth and increasing fetal resorption in midpregnancy. © 2012 Elsevier Inc.
Persistent Identifierhttp://hdl.handle.net/10722/146843
ISSN
2014 Impact Factor: 1.798
2014 SCImago Journal Rankings: 0.840
ISI Accession Number ID
Funding AgencyGrant Number
Research Grant Council (RGC) of the Hong Kong Special Administrative Region, ChinaHKU 7736/07M
Funding Information:

This study was substantially supported by a grant from the Research Grant Council (RGC) of the Hong Kong Special Administrative Region, China (HKU 7736/07M).

References

 

DC FieldValueLanguage
dc.contributor.authorLi, Len_HK
dc.contributor.authorTang, Fen_HK
dc.contributor.authorO, WSen_HK
dc.date.accessioned2012-05-23T05:42:29Z-
dc.date.available2012-05-23T05:42:29Z-
dc.date.issued2012en_HK
dc.identifier.citationTheriogenology, 2012, v. 77 n. 9, p. 1846-1853en_HK
dc.identifier.issn0093-691Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/146843-
dc.description.abstractConcentrations of adrenomedullin (ADM) in circulation, the uterus, and corpora lutea (CL) increase during pregnancy. We previously reported a temporal-spatial pattern of ADM level and gene expression of Adm and its receptor components, from early pregnancy through midpregnancy to late pregnancy in rats. Two earlier reports using an in vivo model of ADM antagonism demonstrated the important roles of ADM in the post-implantation period. Treatment with ADM receptor blocker hADM22-52 starting from gestation Day 8 or Day 14 resulted in fetal-placental growth restriction and reduction in litter size. In this study, the endogenous ADM actions were abolished in the preimplantation period by infusing the antagonist for the ADM receptor (hADM22-52) with the osmotic (Alzet) pump from Days 1-4 of pregnancy. We inferred that ADM, acting through the ADM receptor, had critical roles during preimplantation, as brief inhibition of ADM action by hADM22-52 during this period reduced litter size by restricting placental growth and increasing fetal resorption in midpregnancy. © 2012 Elsevier Inc.en_HK
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/theriogenologyen_HK
dc.relation.ispartofTheriogenologyen_HK
dc.subjectAdrenomedullinen_HK
dc.subjectFemale infertilityen_HK
dc.subjectFetal developmenten_HK
dc.subjectFetal resorptionen_HK
dc.subjectImplantationen_HK
dc.titlePreimplantation antagonism of adrenomedullin action compromises fetoplacental development and reduces litter sizeen_HK
dc.typeArticleen_HK
dc.identifier.emailO, WS:owaisum@hkucc.hku.hken_HK
dc.identifier.authorityO, WS=rp00315en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.theriogenology.2011.12.030en_HK
dc.identifier.pmid22365702-
dc.identifier.scopuseid_2-s2.0-84860475603en_HK
dc.identifier.hkuros199648en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84860475603&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume77en_HK
dc.identifier.issue9en_HK
dc.identifier.spage1846en_HK
dc.identifier.epage1853en_HK
dc.identifier.isiWOS:000304231600013-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLi, L=36071951300en_HK
dc.identifier.scopusauthoridTang, F=54947857500en_HK
dc.identifier.scopusauthoridO, WS=6701729369en_HK
dc.identifier.citeulike10399065-

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