Partial characterization of the embryo-derived platelet-activating factor in mice

O’Neill, Christopher

doi:10.1530/jrf.0.0750375

Cited by 147 publications

(53 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These results indicate that the PRLR must trigger a signal that occurs earlier than prolactin-induced trophic support of the corpus luteum. Candidates include ovum factor, now identified as platelet activating factor (PAF), released by the fertilized eggs (O'Neill 1985), and early pregnancy factor (EPF), a multifactorial activity comprised of PAF, thirodoxin (Orozco et al 1994), chaperonin 10 (Cavanagh andMorton 1994), and other uncharacterized molecules produced by the platelets of the oviduct and ovary in response to embryonic PAF (Sueoka et al 1988). EPF is present in serum 24 hr after ovulation and stimulates lymphocytes to produce a suppressor of the delayed-type hypersensitivity reaction, potentially protecting the ovum from the maternal immune system and promoting embryo cleavage, in addition to acting as a growth factor (Morton et al 1992).…”

Section: Fertilization and Preimplantation Developmentmentioning

confidence: 99%

Null mutation of the prolactin receptor gene produces multiple reproductive defects in the mouse.

Ormandy¹,

Camus²,

Barra³

et al. 1997

Genes Dev.

720

429

View full text Add to dashboard Cite

Mice carrying a germ-line null mutation of the prolactin receptor gene have been produced by gene targeting in embryonic stem cells. Heterozygous females showed almost complete failure of lactation attributable to greatly reduced mammary gland development after their first, but not subsequent, pregnancies. Homozygous females were sterile owing to a complete failure of embryonic implantation. Moreover, they presented multiple reproductive abnormalities, including irregular cycles, reduced fertilization rates, defective preimplantation embryonic development, and lack of pseudopregnancy. Half of the homozygous males were infertile or showed reduced fertility. This work establishes the prolactin receptor as a key regulator of mammalian reproduction, and provides the first total ablation model to further study the role of the prolactin receptor and its ligands.

show abstract

Section: Fertilization and Preimplantation Developmentmentioning

confidence: 99%

Null mutation of the prolactin receptor gene produces multiple reproductive defects in the mouse.

Ormandy¹,

Camus²,

Barra³

et al. 1997

Genes Dev.

720

429

View full text Add to dashboard Cite

show abstract

“…A role for PAF in early pregnancy was suggested when a phospholipid homologous to I-o-alkyl-2-acetyl-i«-glyceryl-3-phosphocholine (PAF) was shown to be produced by mouse (O'Neill, 1985) and human (Collier et ai, 1988) preimplantation embryos. The production of PAF by human embryos after in-vitro fertilization was positively correlated with their pregnancy potential following embryo transfer (O'Neill & Saunders, 1984;O'Neill et ai, 1987).…”

Section: Introductionmentioning

confidence: 99%

Oxidative metabolism of energy substrates by preimplantation mouse embryos in the presence of platelet-activating factor

Ryan

O’Neill²,

Wales³

1990

Reproduction

Self Cite

View full text Add to dashboard Cite

show abstract

“…The binding of Paf to the platelet-activating factor receptor (PTAFR), a member of the G protein-coupled receptor family, accounts for many of the reported actions of Paf (Ishii et al 2002). Paf is produced and released by embryos during preimplantation development of all eutherian species studied to date: mouse (O'Neill 1985, Ryan et al 1989, Roudebush et al 2002, rabbit (Minhas et al 1993), sheep (Battye et al 1991), hamster (Velasquez et al 1995) and human (Collier et al 1990, Nakatsuka et al 1992. No embryos of marsupial species have yet been examined, although Paf appears to be produced by the endometrium of the tammar during the period of reactivation (Kojima et al 1993).…”

Section: Introductionmentioning

confidence: 99%

Paf receptor expression in the marsupial embryo and endometrium during embryonic diapause

et al. 2014

View full text Add to dashboard Cite

The control of reactivation from embryonic diapause in the tammar wallaby (Macropus eugenii) involves sequential activation of the corpus luteum, secretion of progesterone that stimulates endometrial secretion and subsequent changes in the uterine environment that activate the embryo. However, the precise signals between the endometrium and the blastocyst are currently unknown. In eutherians, both the phospholipid Paf and its receptor, platelet-activating factor receptor (PTAFR), are present in the embryo and the endometrium. In the tammar, endometrial Paf release in vitro increases around the time of the early progesterone pulse that occurs around the time of reactivation, but whether Paf can reactivate the blastocyst is unknown. We cloned and characterised the expression of PTAFR in the tammar embryo and endometrium at entry into embryonic diapause, during its maintenance and after reactivation. Tammar PTAFR sequence and protein were highly conserved with mammalian orthologues. In the endometrium, PTAFR was expressed at a constant level in the glandular epithelium across all stages and in the luminal epithelium during both diapause and reactivation. Thus, the presence of the receptor appears not to be a limiting factor for Paf actions in the endometrium. However, the low levels of PTAFR in the embryo during diapause, together with its up-regulation and subsequent internalisation at reactivation, supports earlier results suggesting that endometrial Paf could be involved in reactivation of the tammar blastocyst from embryonic diapause.

show abstract

Partial characterization of the embryo-derived platelet-activating factor in mice

Abstract: Summary. The platelet-activating factor (PAF) produced by mouse embryos showed similar kinetics of action and dose\p=n-\responsecurve, in a bioassay, as did 1-0-alkyl-2\x=req-\ acetyl-sn-glyceryl-3-phosphocholine (PAF-acether

Cited by 147 publications

References 8 publications

Null mutation of the prolactin receptor gene produces multiple reproductive defects in the mouse.

Null mutation of the prolactin receptor gene produces multiple reproductive defects in the mouse.

Oxidative metabolism of energy substrates by preimplantation mouse embryos in the presence of platelet-activating factor

Paf receptor expression in the marsupial embryo and endometrium during embryonic diapause

Contact Info

Product

Resources

About