Prolactin: The Hypophyseal Factor That Terminates Embryonic Diapause in Mink

Murphy, Bruce D.; Concannon, Patrick W.; Travis, H. F.; Hansel, William

doi:10.1095/biolreprod25.3.487

Cited by 86 publications

(54 citation statements)

References 18 publications

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“…In the mink, the increase in cell size was followed by an increase in cell number; it was not possible to determine whether the increase in number resulted from luteal cell divisions, never observed in other species, or from the luteinization of new cells, as described in the sheep (Schwall et al, 1986). Neither prolactin, which is luteotrophic in the mink (Papke et al, 1980;Martinet et al, 1981;Murphy et al, 1981), nor LH, FSH or combinations of these hormones increased the production of progesterone. However, after implantation in the mink , as in the ferret (McKibbin et al, 1984), prolactin and LH interact with low-density lipoproteins to increase the in-vitro production of progesterone by luteal cells.…”

Section: Discussionmentioning

confidence: 99%

Patterns of plasma progesterone, androgen and oestrogen concentrations and in-vitro ovarian steroidogenesis during embryonic diapause and implantation in the mink (Mustela vison)

Stoufflet¹,

Mondain-Monval²,

Simon³

et al. 1989

Reproduction

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Summary. Peripheral plasma progesterone concentrations exhibited an increase 10 days before implantation, coinciding with the resumption of blastocyst growth and with a decrease in plasma androgen values (DHA, androstenedione, testosterone). No definite pattern of oestrone was observed and oestradiol concentrations remained undetectable. The production of steroids by dispersed luteal cells showed that the growth of the corpora lutea paralleled that of blastocysts and resulted in hypertrophy followed by hyperplasia of the luteal cell. The production of progesterone in the medium increased with blastocyst size up to implantation; it was enhanced by mink charcoal-treated serum, but prolactin, LH, FSH or a combination of these hormones did not affect the progesterone production, whatever the stage of diapause. DHA and androstenedione secretion increased in the two last stages of blastocyst growth and was enhanced by LH. The conversion of androstenedione and testosterone into oestrone and oestradiol was observed at all stages of embryonic diapause, indicating that corpora lutea contain aromatase activity even at an early stage. The secretion of oestrone was higher than that of oestradiol. The non-luteal tissue contributed up to 50% of the steroid production; while progesterone and androgen production remained constant, that of oestradiol decreased at the end of the delay period. These results indicated a change in the size and the secretory capacity of the luteal cell related to blastocyst development and implantation. Although progesterone was the main product of the corpora lutea, androgens and oestrogens were also secreted.

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Section: Discussionmentioning

confidence: 99%

Patterns of plasma progesterone, androgen and oestrogen concentrations and in-vitro ovarian steroidogenesis during embryonic diapause and implantation in the mink (Mustela vison)

Stoufflet¹,

Mondain-Monval²,

Simon³

et al. 1989

Reproduction

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“…Females were mated twice, 7 days apart, during the first 2 weeks of March, according to standard husbandry procedures. We and others have shown that prolactin injections terminate obligate embryonic diapause and induce embryo activation and implantation in the mink (32)(33)(34), and a standard protocol consisting of daily intramuscular injections of 1 mg/kg prolactin (Sigma) was employed beginning 1 week following last mating and continuing for 12 days. Implantation takes place approximately on the 13th day after the initiation of prolactin injections, verified by the presence of uterine swellings and histological evidence of trophoblast invasion.…”

Section: Methodsmentioning

confidence: 99%

Transcriptional Regulation of Uterine Vascular Endothelial Growth Factor during Early Gestation in a Carnivore Model, Mustela vison

Lopes

Desmarais

Ledoux

et al. 2006

Journal of Biological Chemistry

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Vascular endothelial growth factor (VEGF) is an essential angiogenic signaling element that acts through its two tyrosine kinase receptors, inducing both proliferation of endothelial cells and vascular permeability. Given the importance of vasculogenesis and angiogenesis to early pregnancy, it is of interest to understand the mechanisms regulating vascular development at this stage. We previously demonstrated that VEGF and receptors are up-regulated during embryo implantation in an unique animal model, the mink, a species displaying obligate embryonic diapause. Herein we examined the role of prostaglandin E2 (PGE 2 ) as a regulator of VEGF during early pregnancy and established the mechanisms of this regulation. We demonstrate that activated embryos secrete PGE 2 and that expression of PGE synthase protein in the uterus is dependent upon direct contact with invading trophoblast cells during implantation. Using mink uterine stromal cells transfected with mink VEGF promoter driving the luciferase reporter gene, we show that PGE 2 induces promoter transactivation and that this response can be eliminated by blockade of protein kinase A. Treatment with antagonists to PGE 2 receptors EP2 and EP4 eliminated the PGE 2 -induced response in transfected cells. Deletional studies of the promoter revealed that a region of 99 bp upstream of the transcription start site is required for PGE 2 -induced transactivation. Mutation of an AP2/Sp1 cluster, found within the 99 bp, completely eliminated the PGE 2 response. Furthermore, chromatin immunoprecipitation assays confirmed binding of the AP2 and Sp1 transcription factors to the endogenous mink VEGF promoter in uterine cells. PGE 2 stimulated acetylation of histone H3 associated with the promoter region containing the AP2/Sp1 cluster. Taken together, these results demonstrate that PGE 2 plays an important role in regulating uterine and thus placental vascular development, acting through its receptors EP2 and EP4, provoking protein kinase A activation of AP2 and Sp1 as well as acetylation of histone H3 to transactivate the VEGF promoter.

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“…Withdrawal of the dopamine agonist (Papke et al 1980) or administration of dopamine antagonists (Murphy 1983) terminates diapause in mink. Indeed, prolactin alone induced implantation in hypophysectomized mink (Murphy et al 1981), as did administration of prolactin to animals in protracted diapause due to chronic melatonin treatment (Murphy et al 1990). In macropod marsupials, prolactin plays an inhibitory role.…”

Section: Control By the Pituitary Glandmentioning

confidence: 99%

Embryonic diapause and its regulation

Lopes¹,

Desmarais²,

Murphy³

2004

Reproduction

183

165

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Embryonic diapause, a condition of temporary suspension of development of the mammalian embryo, occurs due to suppression of cell proliferation at the blastocyst stage. It is an evolutionary strategy to ensure the survival of neonates. Obligate diapause occurs in every gestation of some species, while facultative diapause ensues in others, associated with metabolic stress, usually lactation. The onset, maintenance and escape from diapause are regulated by cascades of environmental, hypophyseal, ovarian and uterine mechanisms that vary among species and between the obligate and facultative condition. In the bestknown models, the rodents, the uterine environment maintains the embryo in diapause, while estrogens, in combination with growth factors, reinitiate development. Mitotic arrest in the mammalian embryo occurs at the G0 or G1 phase of the cell cycle, and may be due to expression of a specific cell cycle inhibitor. Regulation of proliferation in non-mammalian models of diapause provide clues to orthologous genes whose expression may regulate the reprise of proliferation in the mammalian context.

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Prolactin: The Hypophyseal Factor That Terminates Embryonic Diapause in Mink

Cited by 86 publications

References 18 publications

Patterns of plasma progesterone, androgen and oestrogen concentrations and in-vitro ovarian steroidogenesis during embryonic diapause and implantation in the mink (Mustela vison)

Patterns of plasma progesterone, androgen and oestrogen concentrations and in-vitro ovarian steroidogenesis during embryonic diapause and implantation in the mink (Mustela vison)

Transcriptional Regulation of Uterine Vascular Endothelial Growth Factor during Early Gestation in a Carnivore Model, Mustela vison

Embryonic diapause and its regulation

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