Increased Cleaved Caspase-3 Expression in the Prepartum Cervix of Mice

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Preterm birth is a global epidemic and spontaneous preterm birth has no consistent treatment. The cervix acts as a barrier between fetus and vagina and transitions through an inflammatory remodeling process including softening, ripening, and dilation before delivery. Decreased cell nuclei density has been observed in the cervix of pregnant mammals compared to nonpregnant controls during the shift from a soft to a ripened cervix. Whether cervix stromal cells are fewer in number per area due to edema, hypertrophy, or apoptosis as pregnancy progresses to term or with preterm birth is not known. By using immunohistochemistry (IHC) and the specific marker cleaved (c)-Caspase-3, apoptotic cell densities were assessed in cervices from nonpregnant mice, prepartum control mice on days 15, 16.5, 17, or 18 postbreeding (term=day19), and a preterm-birth-induced mouse model on day 16.5 after treatment with progesterone receptor (PR) antagonist RU486, which induces birth 24-hours after injection. The density of cell nuclei/area was the same among pregnant mice whether vehicle-or RU486- treated. The density of cCaspase-3 cells increased to the same extent on the day before birth in mice given either vehicle (day 18) or RU486 (day 16.5) compared to vehicle-treated mice on day 16.5 postbreeding (p<0.05). However, increased apoptosis cannot account for remodeling during the shift from softening to ripened (days 15-17 postbreeding in controls). Quantifying levels of apoptosis in the cervix leading up to birth and in preterm-birth-models could help characterize cervical remodeling and lead to treatments in the prevention of premature birth.



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