Alterations in uterine sodium pump abundance may contribute to the onset and progression of term and preterm labor in mice.
OBJECTIVE: Other investigators have shown that reductions in active sodium pump units increase uterine contractility. Therefore, our goal was to determine whether uterine sodium pump abundance is decreased in mouse models of term and preterm labor. STUDY DESIGN: Mice were studied during the final one-third of pregnancy. Other pregnant mice had preterm labor induced with lipopolysaccharide and were studied at timed intervals thereafter. Uterine sodium pump alpha3-isoform messenger RNA and protein were measured. Data were analyzed by analysis of variance. RESULTS: Uterine sodium pump alpha3-isoform messenger RNA fell significantly from day 14 to day 18 and remained low on the day of birth. Uterine sodium pump alpha3-isoform protein levels decreased significantly also. In lipopolysaccharide-induced preterm labor, uterine sodium pump alpha3-isoform protein, but not messenger RNA, decreased significantly. CONCLUSION: Sodium pump alpha3-isoform protein levels decreased in uterus before term labor and lipopolysaccharide-induced preterm labor. These findings are similar to those in humans, which suggests that this mouse model may be useful in the study of the sodium pump in human pregnancy. Reductions in sodium pump number can increase uterine contractile force and may contribute to labor.[1]References
- Alterations in uterine sodium pump abundance may contribute to the onset and progression of term and preterm labor in mice. Vance, C.J., Esplin, M.S., Hamblin, S., Graves, S.W. Am. J. Obstet. Gynecol. (2006) [Pubmed]
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