Prostaglandins, Indomethacin and the Decidual Cell Reaction in the Mouse Uterus

Rankin, J. C.; Ledford, Barry E.; Jonsson, Haldor T.; Baggett, Billy

doi:10.1095/biolreprod20.2.399

Cited by 76 publications

(30 citation statements)

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“…Concomitant to implantation, uterine stromal cells surrounding the blastocyst proliferate and differentiate to form the deciduum, which supports the developing embryo before the formation of a functional placenta (21). In mice, decidualization can be experimentally induced by intraluminal oil infusion into a receptive uterus (41). Like the initiation of implantation, Cox-2 is also critical for decidualization and is induced as an immediate-early gene after oil infusion (22).…”

Section: Uterine Cox-2 Protein Levels Are Inversely Correlated With Mmentioning

confidence: 99%

MicroRNA regulation of cyclooxygenase-2 during embryo implantation

Chakrabarty

Tranguch²,

Daikoku³

et al. 2007

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

246

213

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The implantation process is complex, requiring reciprocal interactions between implantation-competent blastocysts and the receptive uterus. Because microRNAs (miRNAs) have major roles in regulating gene expression, we speculated that they participate in directing the highly regulated spatiotemporally expressed genetic network during implantation. Here, we show that two miRNAs, mmu-miR-101a and mmu-miR-199a*, are spatiotemporally expressed in the mouse uterus during implantation coincident with expression of cyclooxygenase-2, a gene critical for implantation. More interestingly, our in vitro gain-and loss-of-function experiments show that cyclooxygenase-2 expression is posttranscriptionally regulated by these two miRNAs. We report on miRNAmediated regulation of uterine gene expression in the context of implantation. We believe that many other critical genes related to this process are also regulated by miRNAs. Thus, elucidating the physiological roles of uterine miRNAs will help us better understand the genetic control of implantation, the gateway to a successful pregnancy.mouse ͉ uterus ͉ blastocyst ͉ decidua M icroRNAs (miRNAs) are a novel family of small (Ϸ19-22 nt) noncoding RNAs transcribed by genomes of most metazoa. They are diverse in sequence, evolutionary widespread, and involved in sequence-specific posttranscriptional gene regulation by affecting mRNA stability and/or translation (1-3). In mammals, mature miRNAs are generated via a unique biosynthetic cascade involving RNA polymerase II, nuclear and cytosolic RNase III endonucleases, and their dsRNA binding protein partners. miRNA-guided RNA silencing is executed by a RNA-induced silencing complex (RISC) that involves an interaction between a mature miRNA and its binding site located at the 3Ј

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Section: Uterine Cox-2 Protein Levels Are Inversely Correlated With Mmentioning

confidence: 99%

MicroRNA regulation of cyclooxygenase-2 during embryo implantation

Chakrabarty

Tranguch²,

Daikoku³

et al. 2007

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

246

213

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“…Indomethacin has been known to inhibit the activity of some enzymes including prostaglandin synthetase (Flower and Vane 1974), and reduces the biosynthesis of prostaglandins in each organ (Vane 1971 Rankin et al 1979). Although others have described this inhibitory action of indomethacin, they claimed that indomethacin does not reduce the number of implantation site but affects the embryonal growth after implantation (Hoffman 1978 ;Lundkvist and Nilsson 1980).…”

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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“…Prostaglandins of the E and I series are stimulators of cAMP synthesis in a number of cell types (Kuehl et al 1976;Singhal et al 1976;Goff et al 1978;Omini et al 1979) and artificial deciduogenic stimuli bring about a rapid increase in uterine cAMP levels (Leroy et al 1974;Rankin et al 1977Rankin et al , 1979Kennedy 1983). The increase in uterine cAMP concentrations in response to deciduogenic stimuli is inhibited by indomethacin, suggesting that the response is prostaglandin-mediated Kennedy 1983).…”

Section: Mode Of Action Of Prostaglandinsmentioning

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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Prostaglandins, Indomethacin and the Decidual Cell Reaction in the Mouse Uterus

Cited by 76 publications

References 0 publications

MicroRNA regulation of cyclooxygenase-2 during embryo implantation

MicroRNA regulation of cyclooxygenase-2 during embryo implantation

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

Embryonic signals and the initiation of blastocyst implanation.

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