Inhibition of Hatching of Mouse Blastocysts in vitro by Prostaglandin Antagonists

Biggers, John D.; Leonov, B. V.; Baskar, John F.; Fried, Josef

doi:10.1095/biolreprod19.3.519

Cited by 86 publications

(36 citation statements)

References 61 publications

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“…Information regarding cellspecific synthesis and hydrolysis of this molecule in the uterus will be required to address this issue. Another possibility is that anandamide serves as a reservoir of arachidonic acid for the generation of prostaglandins (PGs) which are important for embryo development and implantation (39)(40)(41). This is consistent with higher levels of amidohydrolase activity and of PGE 2 in implantation sites (14,41).…”

Section: Resultsmentioning

confidence: 79%

Changes in anandamide levels in mouse uterus are associated with uterine receptivity for embryo implantation

Schmid

Paria

Krebsbach

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

239

166

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Anandamide (N-arachidonoylethanolamine) is an endogenous ligand for both the brain-type (CB1-R) and spleen-type (CB2-R) cannabinoid receptors. This investigation demonstrates that the periimplantation mouse uterus contains the highest levels of anandamide (142-1345 pmol͞ mol lipid P; 1-7 g͞g wet weight) yet discovered in a mammalian tissue. The levels f luctuate with the state of pregnancy; down-regulation of anandamide levels is associated with uterine receptivity, while up-regulation is correlated with uterine refractoriness to embryo implantation. Anandamide levels are highest during the nonreceptive phase in the pseudopregnant uterus and in the interimplantation sites, and lowest at the site of embryo implantation. The lower levels of uterine anandamide at the implantation sites may be a mechanism by which implanting embryos protect themselves from the detrimental effects of this endogenous ligand. We also observed a reduced rate of zona-hatching of blastocysts in vitro in the presence of anandamide, and inhibition of implantation by systemic administration of a synthetic cannabinoid agonist CP 55,940. These adverse effects were reversed by SR141716A, a specific CB1-R antagonist. Taken together, the results suggest that an aberrant synthesis of anandamide and͞or expression of the cannabinoid receptors in the uterus͞embryo may account for early pregnancy failure or female infertility.

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Section: Resultsmentioning

confidence: 79%

Changes in anandamide levels in mouse uterus are associated with uterine receptivity for embryo implantation

Schmid

Paria

Krebsbach

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

239

166

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“…In contrast, Kennedy (18) showed that in the rat PGE 2 but not PGI 2 is a key mediator of increased vascular permeability at the implantation site. Considering the fact that the blastocyst either accumulates (19) or synthesizes PGs (20,21), it has been also shown that PGs affect the glucose metabolism of preimplantation embryos (22) and hatching of the blastocysts (7).…”

mentioning

confidence: 99%

Prostaglandin E2 Is a Product of Induced Prostaglandin-endoperoxide Synthase 2 and Microsomal-type Prostaglandin E Synthase at the Implantation Site of the Hamster

Wang¹,

Su²,

Deb³

et al. 2004

Journal of Biological Chemistry

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Certain uterine prostaglandins (PGs) are elevated at implantation sites and are needed to trigger the events of blastocyst implantation that include blastocyst-uterine attachment and stromal decidualization with vascular permeability changes. Several decades of investigations showed that treatment with PG synthesis inhibitors, prior to or during the time of implantation, resulted in either complete inhibition or a delay in implantation or reduction in the number of implantation sites with diminished decidual tissue. Consistent with these findings, we observed that whereas a selective PG endoperoxide synthase (Ptgs) 1 inhibitor SC-560 failed to inhibit implantation, a selective Ptgs2 inhibitor SC-236 showed significantly reduced number and size of implantation sites in progesterone-treated ovariectomized pregnant hamsters. It is known that Ptgs2 expression and Ptgs2-derived prostacyclin (PGI 2 ) synthesis at implantation sites are needed for implantation in the mouse (a rodent that needs ovarian estrogen for implantation). However, it is unknown which Ptgs and PG synthases produce which PGs at implantation sites of the hamster (a rodent that does not need ovarian estrogen for implantation). Here we demonstrate that as blastocyst implantation proceeds, a reduction in Ptgs1 expression from uterine luminal epithelial cells and a gradual induction in Ptgs2 expression exclusively in luminal epithelial and adjacent decidual cells occurred at implantation sites of hamsters. Results also reveal that PGE 2 , but not PGI 2 , is the major PG at implantation sites where Ptgs2 and microsomal type PGE synthases but not PGI synthases are co-expressed. This elevated uterine PGE 2 at implantation sites may serve to initiate or amplify physiological signals required for specific aspects of the implantation process in hamsters.

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“…Indomethacin, added in vitro, may also show these actions except decreasing uterine prostaglandin synthesis. Some investigators have reported an in vitro inhibitory effect and found that indomethacin added in vitro inhibited the hatching of mouse embryo (Biggers et al 1978 ;Hurst and McFarlane 1981). The mechanism of the inhibition of hatching was considered as follows : The endogenous prostaglandins were decreased by indomethacin, so that the expansion of blastocyst could not occur (Biggers et al 1978).…”

Section: Discussionmentioning

confidence: 99%

“…Some investigators have reported an in vitro inhibitory effect and found that indomethacin added in vitro inhibited the hatching of mouse embryo (Biggers et al 1978 ;Hurst and McFarlane 1981). The mechanism of the inhibition of hatching was considered as follows : The endogenous prostaglandins were decreased by indomethacin, so that the expansion of blastocyst could not occur (Biggers et al 1978). In order to study further the mechanism of the in vitro inhibitory effect of indomethacin on the incorporation of [3H] uridine into RNA, the incorporation rate of embryos incubated in a medium containing indomethacin and prostaglandin F2a was compared with that of embryos incubated in a medium containing indomethacin alone.…”

Section: Discussionmentioning

confidence: 99%

Effect of indomethacin and prostaglandin F2.ALPHA. on incorporation of (3H)uridine by preimplantation mouse embryo.

Uehara

Villee

Hoshiai³

1984

Tohoku J. Exp. Med.

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Inhibition of Hatching of Mouse Blastocysts in vitro by Prostaglandin Antagonists

Abstract: The

Cited by 86 publications

References 61 publications

Changes in anandamide levels in mouse uterus are associated with uterine receptivity for embryo implantation

Changes in anandamide levels in mouse uterus are associated with uterine receptivity for embryo implantation

Prostaglandin E2 Is a Product of Induced Prostaglandin-endoperoxide Synthase 2 and Microsomal-type Prostaglandin E Synthase at the Implantation Site of the Hamster

Effect of indomethacin and prostaglandin F2.ALPHA. on incorporation of (3H)uridine by preimplantation mouse embryo.

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