• Title of article

    Alterations in uterine sodium pump abundance may contribute to the onset and progression of term and preterm labor in mice

  • Author/Authors

    Carlos J. Vance، نويسنده , , M. Sean Esplin، نويسنده , , Stephen Hamblin، نويسنده , , Steven W. Graves، نويسنده ,

  • Issue Information
    روزنامه با شماره پیاپی سال 2006
  • Pages
    8
  • From page
    1407
  • To page
    1414
  • Abstract
    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 α3-isoform messenger RNA and protein were measured. Data were analyzed by analysis of variance. Results Uterine sodium pump α3-isoform messenger RNA fell significantly from day 14 to day 18 and remained low on the day of birth. Uterine sodium pump α3-isoform protein levels decreased significantly also. In lipopolysaccharide-induced preterm labor, uterine sodium pump α3-isoform protein, but not messenger RNA, decreased significantly. Conclusion Sodium pump α3-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.
  • Keywords
    SodiumUterusRNAProteinContractionLaborMouse
  • Journal title
    American Journal of Obstetrics and Gynecology
  • Serial Year
    2006
  • Journal title
    American Journal of Obstetrics and Gynecology
  • Record number

    645768