Article: Complement 3 deficiency impairs early pregnancy in mice

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TitleComplement 3 deficiency impairs early pregnancy in mice
AuthorsChow, WN
Lee, YL
Wong, PC
Chung, MK
Lee, KF
Yeung, WSB1
Issue Date2009
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/37692
CitationMolecular Reproduction And Development, 2009, v. 76 n. 7, p. 647-655 [How to Cite?]
DOI: http://dx.doi.org/10.1002/mrd.21013
AbstractHuman oviductal cells produce complement-3 (C3) and its derivative, iC3b. These molecules are important in immune responses. Our recent study suggested that iC3b also possessed embryotrophic activity and it stimulates the blastulation and hatching rates of in vitro cultured mouse embryos. The objective is to study the impact of C3 deficiency on early pregnancy in vivo using homozygous C3-deficient (C3KO) and wild-type (C3WT) mice. C3 protein was undetectable in the reproductive tissues of C3KO mice. Deficiency in C3 is associated with significantly longer estrous cycle (P = 0.037). No significant difference was found in the ovulation rate, total cell count in blastocysts and implantation rate between the wild-type and the C3KO mice, though C3KO mice tended to have lower values in the latter two parameters. On day 15 of pregnancy, C3KO mice had fewer conceptus (P < 0.001) and higher resorption rate (P < 0.001) than that of C3WT mice. The fetal and placental weights (P < 0.001) were lower in the C3KO mice. The placenta of C3KO mice had smaller spongiotrophoblast (P = 0.001) and labyrinth (P = 0.037). Deficiency in C3 is associated with mild impairment in early pregnancy including longer estrous cycle and higher resorption rates after implantation. The impairment may be related to compromised placental development leading to under-developed fetuses. © 2009 Wiley-Liss, Inc.
ISSN1040-452X
2011 Impact Factor: 2.532
2011 SCImago Journal Rankings: 0.179
DOIhttp://dx.doi.org/10.1002/mrd.21013
ISI Accession Number IDWOS:000266517200007
Funding AgencyGrant Number
Research Grant Council, Hong KongHKU7319/01M
HKU7411/04M
Funding Information:

This work was supported in part by grants (HKU7319/01M to W.S.B.Y. and HKU7411/04M to K.F.L.) from the Research Grant Council, Hong Kong.

ReferencesReferences in Scopus
DC Field
Value
dc.contributor.authorChow, WN
dc.contributor.authorLee, YL
dc.contributor.authorWong, PC
dc.contributor.authorChung, MK
dc.contributor.authorLee, KF
dc.contributor.authorYeung, WSB
dc.date.accessioned2010-09-06T09:24:08Z
dc.date.available2010-09-06T09:24:08Z
dc.date.issued2009
dc.description.abstractHuman oviductal cells produce complement-3 (C3) and its derivative, iC3b. These molecules are important in immune responses. Our recent study suggested that iC3b also possessed embryotrophic activity and it stimulates the blastulation and hatching rates of in vitro cultured mouse embryos. The objective is to study the impact of C3 deficiency on early pregnancy in vivo using homozygous C3-deficient (C3KO) and wild-type (C3WT) mice. C3 protein was undetectable in the reproductive tissues of C3KO mice. Deficiency in C3 is associated with significantly longer estrous cycle (P = 0.037). No significant difference was found in the ovulation rate, total cell count in blastocysts and implantation rate between the wild-type and the C3KO mice, though C3KO mice tended to have lower values in the latter two parameters. On day 15 of pregnancy, C3KO mice had fewer conceptus (P < 0.001) and higher resorption rate (P < 0.001) than that of C3WT mice. The fetal and placental weights (P < 0.001) were lower in the C3KO mice. The placenta of C3KO mice had smaller spongiotrophoblast (P = 0.001) and labyrinth (P = 0.037). Deficiency in C3 is associated with mild impairment in early pregnancy including longer estrous cycle and higher resorption rates after implantation. The impairment may be related to compromised placental development leading to under-developed fetuses. © 2009 Wiley-Liss, Inc.
dc.description.natureLink_to_subscribed_fulltext
dc.identifier.citationMolecular Reproduction And Development, 2009, v. 76 n. 7, p. 647-655 [How to Cite?]
DOI: http://dx.doi.org/10.1002/mrd.21013
dc.identifier.doihttp://dx.doi.org/10.1002/mrd.21013
dc.identifier.epage655
dc.identifier.hkuros158112
dc.identifier.isiWOS:000266517200007
Funding AgencyGrant Number
Research Grant Council, Hong KongHKU7319/01M
HKU7411/04M
Funding Information:

This work was supported in part by grants (HKU7319/01M to W.S.B.Y. and HKU7411/04M to K.F.L.) from the Research Grant Council, Hong Kong.

dc.identifier.issn1040-452X
2011 Impact Factor: 2.532
2011 SCImago Journal Rankings: 0.179
dc.identifier.issue7
dc.identifier.openurl
dc.identifier.pmid19205046
dc.identifier.scopuseid_2-s2.0-67449106491
dc.identifier.spage647
dc.identifier.urihttp://hdl.handle.net/10722/87010
dc.identifier.volume76
dc.languageeng
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/37692
dc.publisher.placeUnited States
dc.relation.ispartofMolecular Reproduction and Development
dc.relation.referencesReferences in Scopus
dc.rightsMolecular Reproduction and Development. Copyright © John Wiley & Sons, Inc.
dc.titleComplement 3 deficiency impairs early pregnancy in mice
dc.typeArticle
Author Affiliations
  1. The University of Hong Kong