Changes in prostaglandin levels in the sensitized and non-sensitized uterus of the mouse after the intrauterine instillation of oil or saline

Milligan, S. R.; Lytton, Fiona D. C.

doi:10.1530/jrf.0.0670373

Cited by 20 publications

(14 citation statements)

References 17 publications

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“…For mice, there are varying reports for the effects of deciduogenic stimuli. Jonsson et al (1979), Rankin et al (1979) and Milligan & Lytton (1983) all found the PGF 2a concentrations to be rapidly increased after stimulation. Jonsson et al (1979) reported that PGE 2 was also increased, while Milligan & Lytton (1983) found PGE 2 as well as PGI 2 to be unchanged.…”

Section: Which Pg?mentioning

confidence: 87%

Prostaglandins and the initiation of blastocyst implantation and decidualization

Kennedy¹,

Gillio-Meina²,

Phang³

2007

Reproduction

137

120

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The process of blastocyst implantation in mammals is remarkably variable, especially in the extent of trophoblast invasion of the endometrium. In most species studied, the earliest macroscopically identifiable sign of blastocyst implantation is an increase in endometrial vascular permeability in areas adjacent to the blastocysts. This is followed in species with invasive implantation by decidualization, again localized to areas adjacent to the blastocysts. In some species, the application of a stimulus to the endometrium can result in increased endometrial vascular permeability and decidualization. Based initially on studies utilizing inhibitors of prostaglandin (PG) synthesis and more recently on studies using the techniques of transgenics, considerable evidence has accumulated indicating that PGs have an important role in the early events of implantation and artificially induced decidualization. However, which PGs are involved remains controversial. There may be differences between species, and different PGs may be involved at different times.

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Section: Which Pg?mentioning

confidence: 87%

Prostaglandins and the initiation of blastocyst implantation and decidualization

Kennedy¹,

Gillio-Meina²,

Phang³

2007

Reproduction

137

120

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“…3). Prostaglandins and cyclic AMP have been strongly implicated as potential mediators of these responses, but their precise role is still unclear (Milligan & Lytton, 1983;Kennedy, 1984). To what extent the transient period of hormone-induced sensitivity to deciduogenic stimuli is dependent on qualitative and/or quantita¬ tive changes in the production of (Kennedy, 1983), or sensitivity to (Kennedy et ai, 1983), such stimuli remains to be clarified.…”

Section: Discussionmentioning

confidence: 99%

The sensitivity of the uterus of the mouse and rat to intraluminal instillation

Milligan¹

1987

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The tissue accumulation of 125I-labelled human serum albumin 30 min after intravenous injection was used as an index of uterine vascular permeability. In ovariectomized mice, all sham and experimental instillation procedures produced a 6-10-fold increase in vascular permeability. Some effects were also manifest in the contralateral, control horn. In ovariectomized rats, instillation of saline and arachis oil increased vascular permeability 3-7-fold. After 3 or more days of progesterone treatment following oestradiol priming, fluorocarbon and arachis oil instillation produced marked vascular responses, but these were not restricted to the transient period in which the uterus would respond with decidualization. An IUD prevented the response to arachis oil instillation. These results indicate that the uterus is very sensitive to any manipulation and are consistent with decidualization representing a specialization of a normal uterine inflammatory response.

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“…Not all data are in agreement; in the hamster, prostaglandins E, but not F, concentrations are elevated at implantation sites (Evans and Kennedy 1978) while in the mouse, uterine concentrations of prostaglandins F, but not E or 12, are elevated in response to a deciduogenic stimulus (Milligan and Lytton 1983). Thus measurements of prostaglandins have not identified a single prostaglandin as the mediator of the endometrial vascular changes.…”

Section: Which Prostaglandins?mentioning

confidence: 96%

“…In addition, oestrogens in low dosages act synergistically with progesterone to sensitize the rat and mouse uterus for the decidual cell reaction (Yochim and De Feo 1963;Armstrong and King 1971;Finn and Porter 1975). That these changes in uterine sensitization might be related to the ability of the uterus to produce prostaglandins has been investigated but the results indicate that uterine prostaglandin levels in response to a standardized artificial stimulus does not provide a ready explanation for the changes in sensitization (Kennedy 1980a(Kennedy , 1980bMilligan and Lytton 1983). Rather, maximum uterine sensitization corresponded with the maximum ability of the endometrium to respond to intrauterine-injected prostaglandin E2 with increased endometrial vascular permeability (Kennedy 1980a(Kennedy , 1980b.…”

Section: Control Of Uterine Sensitizationmentioning

confidence: 99%

Embryonic signals and the initiation of blastocyst implanation.

Kennedy¹

1983

Aust. Jnl. Of Bio. Sci.

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The earliest sign of blastocyst implantation is an increase in endometrial vascular permeability which is localized in areas adjacent to blastocysts. The localized nature of this response suggests that it occurs in response to a signal from the blastocyst. It has been suggested that this signal may be physical in nature, or may be due to blastocyst-produced histamine, oestrogen or prostaglandins. The evidence for each of these is reviewed. At present, it is not possible to exclude any of these signals, which are not mutually exclusive, with certainty. The bulk of the evidence suggests that prostaglandins have an obligatory role in the initiation of implantation, but they may not necessarily be of blastocyst origin.

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Changes in prostaglandin levels in the sensitized and non-sensitized uterus of the mouse after the intrauterine instillation of oil or saline

Cited by 20 publications

References 17 publications

Prostaglandins and the initiation of blastocyst implantation and decidualization

Prostaglandins and the initiation of blastocyst implantation and decidualization

The sensitivity of the uterus of the mouse and rat to intraluminal instillation

Embryonic signals and the initiation of blastocyst implanation.

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