title: Influence of the preimplantation embryo development (Ped) gene on embryonic platelet-activating factor (PAF) levels.
abstract: OBJECTIVE
  A major gene responsible for the control of preimplantation cleavage rate is the Ped gene, the product of which is the Qa-2 protein. Fast, but not slow developing mouse embryos express the Qa-2 protein. Platelet-activating factor (PAF) is a novel and potent signaling phospholipid that has unique pleiotropic properties in addition to platelet activation. PAF plays a significant role in virtually every reproductive event, including ovulation, fertilization, implantation, and parturition. The role of the Ped gene in PAF production by preimplantation embryos is yet to be established. The presence of this gene provides embryos with a reproductive advantage over those that are Ped negative, and may also serve as a regulator of PAF synthesis. The study hypothesis is that the amount of PAF produced is dependent upon the presence or absence of the Ped gene.
  
  
  METHODS
  B6.K1 (Ped negative) and B6.K2 (Ped positive) mouse embryo-conditioned culture media were assayed for PAF content by a PAF-specific radioimmunoassay.
  
  
  RESULTS
  There was a significant (p < 0.001) difference in blastocyst development rates between the Ped+ B6.K2 (61.0%) and the Ped- B6.K1 (25.3%) embryo culture groups. There was a significant difference (p < 0.05) in PAF production between the Ped+ B6.K2 (4.70+/-0.46 pmol per embryo) embryo culture group and the Ped- B6.K1 (10.02+/-3.49 pmol per embryo) embryo group. The B6.K1 (Ped-) embryo group produced >2x more PAF than did the B6.K2 (Ped+) group.
  
  
  CONCLUSIONS
  The Ped gene plays a role in PAF production and release in preimplantation stage embryos. The use of two mouse identical strains, except for the Ped gene, show that its presence is associated with an increase in developmental potential. Embryos where the Ped gene was absent produced significantly higher levels of PAF, which may aid in their survival.
authors.affiliation: Savannah State University, Savannah, Georgia, USA.
authors.forename: Elissa T
authors.initials: ET
authors.lastname: Purnell
authors.forename: Carol M
authors.initials: CM
authors.lastname: Warner
authors.forename: Hilton I
authors.initials: HI
authors.lastname: Kort
authors.forename: Dorothy
authors.initials: D
authors.lastname: Mitchell-Leef
authors.forename: Carlene W
authors.initials: CW
authors.lastname: Elsner
authors.forename: Daniel B
authors.initials: DB
authors.lastname: Shapiro
authors.forename: Joe B
authors.initials: JB
authors.lastname: Massey
authors.forename: William E
authors.initials: WE
authors.lastname: Roudebush
mesh_terms: D000818:Animals; D001755:Blastocyst / Q000502:physiology; D047108:Embryonic Development; D005260:Female; D018507:Gene Expression Regulation, Developmental; D015395:Histocompatibility Antigens Class I / Q000235:genetics* / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D010972:Platelet Activating Factor / Q000378:metabolism*; D011247:Pregnancy
chemical_list: D015395:Histocompatibility Antigens Class I; D010972:Platelet Activating Factor; C032907:Q surface antigens