Presentation Title

Progesterone treatment delays birth at term, but not cervix ripening

Faculty Mentor

Steven M. Yellon Phd, Loma Linda University

Start Date

17-11-2018 12:30 PM

End Date

17-11-2018 2:30 PM

Location

HARBESON 45

Session

POSTER 2

Type of Presentation

Poster

Subject Area

health_nutrition_clinical_science

Abstract

During pregnancy, the cervix serves as a gatekeeper to maintain pregnancy and a barrier to birth. For parturition to occur, the cervix remodels through an inflammatory process that involves softening and ripening. Evidence suggests that loss of progesterone (P4) effectiveness leads to cervix ripening, as characterized by reduced cell nuclei density, increased presence of macrophages, and degradation of collagen in cross-linked fibers, well before birth at term when P4 concentrations in blood are near or at peak. The hypothesis that P4 supplements will not delay birth or ripening past term was the focus of the present study. Accordingly, pregnant mice were implanted with silastic capsules with vehicle or P4 (1g/ml sesame oil, s.c.) on day 16 postbreeding. Serum P4 and cervix histology were studied thereafter to assess ripening using stains as previously described (PMID27233754). Compared to vehicle controls that gave birth by the morning of day 19 or 20 postbreeding (n=9), P4-treated mice delayed birth to Day 22 when the study concluded (n=10). In mice given vehicle, serum P4 declined 1-2 days before birth; p<0.05 ANOVA, n=3-5/group), while P4 treatment was at peak or higher concentrations. Analyses of cervix sections indicate P4 treatment did not affect the densities of cell nuclei or macrophages/cell nuclei (n=3-5/group). These results suggest that P4 treatment may override the mechanism for labor and delivery at term, but not the progression of cervix ripening that appears to result from loss of P4 efficacy. The possibility that mechanisms for labor and cervix ripening are differentially regulated has potential applications for development of therapeutic approaches to arrest preterm birth or facilitate delivery when parturition is delayed or hampered by incomplete remodeling of the cervix. Supported in part by NIH R01HD054931.

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Nov 17th, 12:30 PM Nov 17th, 2:30 PM

Progesterone treatment delays birth at term, but not cervix ripening

HARBESON 45

During pregnancy, the cervix serves as a gatekeeper to maintain pregnancy and a barrier to birth. For parturition to occur, the cervix remodels through an inflammatory process that involves softening and ripening. Evidence suggests that loss of progesterone (P4) effectiveness leads to cervix ripening, as characterized by reduced cell nuclei density, increased presence of macrophages, and degradation of collagen in cross-linked fibers, well before birth at term when P4 concentrations in blood are near or at peak. The hypothesis that P4 supplements will not delay birth or ripening past term was the focus of the present study. Accordingly, pregnant mice were implanted with silastic capsules with vehicle or P4 (1g/ml sesame oil, s.c.) on day 16 postbreeding. Serum P4 and cervix histology were studied thereafter to assess ripening using stains as previously described (PMID27233754). Compared to vehicle controls that gave birth by the morning of day 19 or 20 postbreeding (n=9), P4-treated mice delayed birth to Day 22 when the study concluded (n=10). In mice given vehicle, serum P4 declined 1-2 days before birth; p<0.05 ANOVA, n=3-5/group), while P4 treatment was at peak or higher concentrations. Analyses of cervix sections indicate P4 treatment did not affect the densities of cell nuclei or macrophages/cell nuclei (n=3-5/group). These results suggest that P4 treatment may override the mechanism for labor and delivery at term, but not the progression of cervix ripening that appears to result from loss of P4 efficacy. The possibility that mechanisms for labor and cervix ripening are differentially regulated has potential applications for development of therapeutic approaches to arrest preterm birth or facilitate delivery when parturition is delayed or hampered by incomplete remodeling of the cervix. Supported in part by NIH R01HD054931.