Complement 3 deficiency impairs early pregnancy in mice

Wang Ngai Chow, Yin Lau Lee, Po Chau Wong, Man Kin Chung, Kai Fai Lee, William Shu Biu Yeung

Research output: Journal article publicationJournal articleAcademic researchpeer-review

37 Citations (Scopus)


Human 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.

Original languageEnglish
Pages (from-to)647-655
Number of pages9
JournalMolecular Reproduction and Development
Issue number7
Publication statusPublished - Jul 2009
Externally publishedYes

ASJC Scopus subject areas

  • Genetics
  • Developmental Biology
  • Cell Biology


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