title: The molecular mechanisms of cervical ripening differ between term and preterm birth.
abstract: 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.
authors.affiliation: Cecil H. and Ida Green Center for Reproductive Biology Sciences, Department of Obstetrics and Gynecology, The University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-9032, USA.
authors.forename: Roxane
authors.initials: R
authors.lastname: Holt
authors.forename: Brenda C
authors.initials: BC
authors.lastname: Timmons
authors.forename: Yucel
authors.initials: Y
authors.lastname: Akgul
authors.forename: Meredith L
authors.initials: ML
authors.lastname: Akins
authors.forename: Mala
authors.initials: M
authors.lastname: Mahendroo
mesh_terms: D000818:Animals; D020070:Cervical Ripening / Q000187:drug effects / Q000502:physiology*; D002584:Cervix Uteri / Q000473:pathology; D005260:Female; D005786:Gene Expression Regulation / Q000502:physiology; D006727:Hormone Antagonists / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000633:toxicity; D051379:Mice; D015735:Mifepristone / Q000494:pharmacology; D011247:Pregnancy; D047928:Premature Birth; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D006727:Hormone Antagonists; D008070:Lipopolysaccharides; D015735:Mifepristone