Alterations in uterine sodium pump abundance may contribute to the onset of mouse labor
Alterations in uterine sodium pump abundance may contribute to the onset of mouse labor
ONSET OF MOUSE LABOR CARLOS VANCE II, STEVEN HAMBLIN, MICHAEL ESPLIN, STEVEN GRAVES, Brigham Young University, Chemistry and Biochemistry, Provo, Utah, University of Utah, Obstetrics and Gynecology, Salt Lake City, Utah OBJECTIVE: Reductions in sodium pump (SP) abundance increase uterine contractile activity. We described a reduction in uterine SPa3 isoform in pregnant women in active labor, however those studies could not determine whether the change occurred before or resulted from labor. To determine whether the mouse might serve as a model for human pregnancy in terms of the SP and to determine whether changes in SP anticipate (and hence potentially increase uterine contractility) or follow labor, we studied pregnant mice over their final trimester. STUDY DESIGN: Pregnant C57Bl6 mice were sacrificed (n = 4) at 14, 16 and 18 days gestation, during birth (wday 19) and 1 day post partum, uterus harvested and RNA isolated for rtPCR. cDNA was obtained by reverse transcriptase. Samples were amplified and quantified using an ABI 7900HT instrument using mouse SPa3 primers. Western Blot analysis using a SPa3 isoform specific monoclonal antibody was also done. Data were analyzed by ANOVA with post hoc Newman-Keuls’ pair-wise comparisons. RESULTS: SPa3 isoform mRNA was most abundant on day 14 (9.4 G 0.3 ! 10-7 units), was lower day 16 (8.0 G 1.1 ! 10-7 units) and significantly lower day 18 (4.5 G 0.6 ! 10-7 units) and at birth (wday 19, 3.7 G 0.1 ! 10-7 units). SPa3 rose significantly post delivery (7.5 G 1.7 ! 10-7 units). The overall trend was significant (P = .004). Western blot analysis demonstrated a similar but delayed pattern. CONCLUSION: Mouse uterine SPa3 isoform protein expression fell prior to labor and appeared to be mediated by reductions in mRNA. These reductions parallel changes observed in term pregnant women. Such reductions increase uterine contractile activity and may be a fundamental mechanism in mouse and human labor. SMFM Abstracts S187
- Brigham Young University Idaho United States
- University of Utah United States
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