The Molecular Mechanisms of Cervical Ripening Differ between Term and Preterm Birth

Premature cervical ripening can occur by more than one mechanism, and premature ripening associated with preterm birth is not simply an acceleration of term ripening. In the current study, the mechanisms of premature cervical ripening in murine models of preterm birth resulting from infection or ear...

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Veröffentlicht in:Endocrinology (Philadelphia) 2011-03, Vol.152 (3), p.1036-1046
Hauptverfasser: Holt, Roxane, Timmons, Brenda C, Akgul, Yucel, Akins, Meredith L, Mahendroo, Mala
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creator Holt, Roxane
Timmons, Brenda C
Akgul, Yucel
Akins, Meredith L
Mahendroo, Mala
description Premature cervical ripening can occur by more than one mechanism, and premature ripening associated with preterm birth is not simply an acceleration of term ripening. In the current study, the mechanisms of premature cervical ripening in murine models of preterm birth resulting from infection or early progesterone withdrawal were compared with the process of term cervical ripening. Tissue morphology, weight, gene expression, and collagen content along with immune cell populations were evaluated. Premature ripening induced by the progesterone receptor antagonist mifepristone results from an acceleration of processes in place during term ripening as well as partial activation of proinflammatory and immunosuppressive processes observed during postpartum repair. In contrast to term or mifepristone-induced preterm ripening, premature ripening induced in an infection model occurs by a distinct mechanism which is dominated by an influx of neutrophils into the cervix, a robust proinflammatory response and increased expression of prostaglandin-cyclooxygenase-endoperoxide synthase 2, important in prostaglandin biosynthesis. Key findings from this study confirm that cervical ripening can be initiated by more than one mechanism and is not necessarily an acceleration of the physiologic process at term. These results will influence current strategies for identifying specific etiologies of preterm birth and developing subsequent therapies.
doi_str_mv 10.1210/en.2010-1105
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In the current study, the mechanisms of premature cervical ripening in murine models of preterm birth resulting from infection or early progesterone withdrawal were compared with the process of term cervical ripening. Tissue morphology, weight, gene expression, and collagen content along with immune cell populations were evaluated. Premature ripening induced by the progesterone receptor antagonist mifepristone results from an acceleration of processes in place during term ripening as well as partial activation of proinflammatory and immunosuppressive processes observed during postpartum repair. In contrast to term or mifepristone-induced preterm ripening, premature ripening induced in an infection model occurs by a distinct mechanism which is dominated by an influx of neutrophils into the cervix, a robust proinflammatory response and increased expression of prostaglandin-cyclooxygenase-endoperoxide synthase 2, important in prostaglandin biosynthesis. 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subjects Animal models
Animals
Biological and medical sciences
Biosynthesis
Birth
Cell activation
Cervical Ripening - drug effects
Cervical Ripening - physiology
Cervix Uteri - pathology
Diseases of mother, fetus and pregnancy
Female
Fundamental and applied biological sciences. Psychology
Gene expression
Gene Expression Regulation - physiology
Gynecology. Andrology. Obstetrics
Hormone Antagonists - pharmacology
Immune system
Inflammation
Leukocytes (neutrophilic)
Lipopolysaccharides - toxicity
Medical sciences
Mice
Mifepristone
Mifepristone - pharmacology
Molecular modelling
Pregnancy
Pregnancy. Fetus. Placenta
Premature Birth
Progesterone
Prostaglandin endoperoxide synthase
Quorum sensing
Reproduction-Development
Reverse Transcriptase Polymerase Chain Reaction
Ripening
Vertebrates: endocrinology
title The Molecular Mechanisms of Cervical Ripening Differ between Term and Preterm Birth
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