The Comparative Physiology of Parturition in Mammals: Hormones and Parturition in Mammals

Young, I. R.; Renfree, Marilyn B.; Mesiano, Sam; Shaw, Geoff; Jenkin, Graham; Smith, Roger

doi:10.1016/b978-0-12-374928-4.10006-9

Cited by 23 publications

(25 citation statements)

References 156 publications

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“…38 Human parturition, however, occurs without systemic progesterone withdrawal. Maternal, fetal, and amniotic fluid concentrations of progesterone and HP remain high throughout pregnancy and labor and delivery.…”

Section: Commentmentioning

confidence: 99%

Progesterone inhibits in vitro fetal membrane weakening

Kumar

Springel

Moore

et al. 2015

American Journal of Obstetrics and Gynecology

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Section: Commentmentioning

confidence: 99%

Progesterone inhibits in vitro fetal membrane weakening

Kumar

Springel

Moore

et al. 2015

American Journal of Obstetrics and Gynecology

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“…Social interactions, such as mating and nursing, are enhanced by exogenous oxytocin, reduced by oxytocin receptor blockade, and/or may trigger the release of oxytocin in the brain and periphery (Richard et al, ; Landgraf, ; Nishimori et al, ; Gimpl and Fahrenholz, ). Central release of oxytocin governs important behaviors such as pair bonding and maternal care of infants (Pedersen and Prange, ; McCarthy, ; Young, ; Marlin et al, ). The changes that underlie these behaviors are starting to be addressed at the synaptic level.…”

Section: Introductionmentioning

confidence: 99%

Oxytocin modulation of neural circuits for social behavior

Marlin

Froemke

2016

Developmental Neurobiology

103

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Oxytocin is a hypothalamic neuropeptide that has gained attention for the effects on social behavior. Recent findings shed new light on the mechanisms of oxytocin in synaptic plasticity and adaptively modifying neural circuits for social interactions such as conspecific recognition, pair bonding, and maternal care. Here, we review several of these newer studies on oxytocin in the context of previous findings, with an emphasis on social behavior and circuit plasticity in various brain regions shown to be enriched for oxytocin receptors. We provide a framework that highlights current circuit-level mechanisms underlying the widespread action of oxytocin. © 2016 Wiley Periodicals, Inc. Develop Neurobiol 77: 169-189, 2017.

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“…Progesterone acting via the nuclear progesterone receptor (PR) isoforms, PR-A and PR-B, is essential for the establishment and maintenance of pregnancy and withdrawal of its PR-mediated pro-gestational actions is a principal trigger for parturition (1,2). In all viviparous species examined to date disruption of PR signaling by administration of PR antagonists such as RU486 (mifepristone) or ZK98299 (onapristone), increases myometrial contractility and induces labor and delivery at all stages of pregnancy (3).…”

Section: Introductionmentioning

confidence: 99%

Inflammatory Stimuli Increase Progesterone Receptor-A Stability and Transrepressive Activity in Myometrial Cells

Peters¹,

Yi²,

Skomorovska-Prokvolit³

et al. 2016

Endocrinology

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The steroid hormone progesterone acting via the nuclear progesterone receptor (PR) isoforms, progesterone receptor A (PR-A) and progesterone receptor B (PR-B), is essential for the maintenance of uterine quiescence during pregnancy. Inhibition of PR signaling augments uterine contractility and induces labor. Human parturition is thought to be triggered by modulation of PR signaling in myometrial cells to induce a functional progesterone withdrawal. One mechanism for functional progesterone withdrawal is increased abundance of PR-A, which decreases progesterone responsiveness by inhibiting the transcriptional activity of PR-B. Human parturition also involves tissue-level inflammation within the myometrium. This study examined the control of PR-A abundance and transrepressive activity in myometrial cells and the role of the inflammatory stimuli in the form of interleukin-1β (IL-1β) and lipopolysaccharide (LPS) in these processes. We found that abundance of PR-A was markedly increased by progesterone and by exposure to IL-1β and LPS via posttranslational mechanisms involving increased PR-A protein stability. In contrast, progesterone decreased abundance of PR-B by increasing its rate of degradation. Together, progesterone and proinflammatory stimuli induced a PR-A-dominant state in myometrial cells similar to that observed in term laboring myometrium. IL-1β and LPS also increased the capacity for PR-A to inhibit the transcriptional activity of PR-B. Taken together, our data suggest that proinflammatory stimuli increase the steady-state levels of PR-A and its transrepressive activity in myometrial cells and support the hypothesis that tissue-level inflammation triggers parturition by inducing PR-A-mediated functional progesterone withdrawal.

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The Comparative Physiology of Parturition in Mammals: Hormones and Parturition in Mammals

Cited by 23 publications

References 156 publications

Progesterone inhibits in vitro fetal membrane weakening

Progesterone inhibits in vitro fetal membrane weakening

Oxytocin modulation of neural circuits for social behavior

Inflammatory Stimuli Increase Progesterone Receptor-A Stability and Transrepressive Activity in Myometrial Cells

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