Insights into parturition biology from genetically altered mice
Abstract
With the growing frequency of preterm birth, increased effort has been made to elucidate the physiology of normal and aberrant parturition. As with many developmental processes, the study of genetically altered mice has led to an increased understanding of mechanisms controlling the maintenance and resolution of pregnancy. Studies in genetically altered mice have implicated critical roles for both prostaglandin synthesis and degradation in luteolysis and the progression of labor. The importance of local modulation of progesterone activity to cervical ripening has also been demonstrated. Although a decline in levels of serum progesterone is a part of normal labor initiation in mice but not humans, murine labor without progesterone withdrawal has been reported in some cases. These findings emphasize the importance of other components of the parturition cascade that are shared in mice and humans and highlights the importance of an increased understanding of the physiology of mouse parturition.
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Mice studies demonstrate that during birth, oxytocin operates through a series of pathways that overlap with numerous other hormonal systems such as cortisol and corticotrophin-releasing hormone.
“Mice studies demonstrate that during birth, oxytocin operates through a series of pathways that overlap with numerous other hormonal systems such as cortisol and corticotrophin-releasing hormone (Gross et al., 2000; Ratajczak and Muglia, 2008).”
From The evolved nest, oxytocin functioning, and prosocial development (2023) · cites this paper as Ratajczak and Muglia, 2008
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Misregulated Progesterone Secretion and Impaired Pregnancy in Cyp11a1 Transgenic Mice1
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Self-citationGeneration of myometrium-specific Bmal1 knockout mice for parturition analysis
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“Mice studies demonstrate that during birth, oxytocin operates through a series of pathways that overlap with numerous other hormonal systems such as cortisol and corticotrophin-releasing hormone (Gross et al., 2000; Ratajczak and Muglia, 2008).”
BackgroundActivation of Gq/11 in the Mouse Corpus Luteum Is Required for Parturition
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Self-citationMmp2 Deficiency Leads to Defective Parturition and High Dystocia Rates in Mice
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MMP2 loss leads to defective parturition and severe dystocia in micePreprint
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- Authors
- Ratajczak, C. K., & Muglia, L. J.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Muglia, Louis J
- Venue
- Pediatric Research
- Published
- 2008-12
- Volume
- 64
- Issue
- 6
- Pages
- 581-589
- ISSN
- 0031-3998 (ISSN-L)
- 1530-0447
- OpenAlex
- W2076065642
- Cited by
- 83
- References
- 106
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 3 · 2023: 3 · 2022: 5 · 2021: 6 · 2020: 7 · 2019: 1 · 2018: 8 · 2017: 2 · 2016: 6 · 2015: 5 · 2014: 6 · 2013: 9 · 2012: 4
- FWCI
- 0.50
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Pediatric Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Preterm Birth and Chorioamnionitis
- Health Sciences › Medicine › Obstetrics and Gynecology › Maternal and Perinatal Health Interventions
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Pregnancy-related medical research
- Keywords
- childbirth, labor initiation, preterm birth, genetically modified mice, prostaglandin synthesis, prostaglandin degradation, luteolysis, progesterone withdrawal, cervical ripening, pregnancy maintenance
- MeSH terms
- Animals, Circadian Rhythm, Luteolysis, Female, Humans, Hydroxyprostaglandin Dehydrogenases, Mice, Transgenic, Oxytocin, Pregnancy, Pregnancy, Animal, Progesterone, Prostaglandins, Uterine Contraction, 20-Hydroxysteroid Dehydrogenases, Connexin 43, Cervical Ripening, Potassium Channels, Calcium-Activated, Parturition, Pulmonary Surfactant-Associated Protein A, Premature Birth, Mice
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