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Expression of Myometrial Activation and Stimulation Genes in a Mouse Model of Preterm Labor: Myometrial Activation, Stimulation, and Preterm Labor

Perinatal Research Centre, Departments of Obstetrics and Gynecology (J.L.C., D.B.Z., D.M.O.), [Pediatrics (D.M.O.), and Physiology (D.H.S., D.M.O.), University of Alberta, Edmonton, Canada T6G-2S2

Address all correspondence and requests for reprints to: Jocelynn L. Cook, Ph.D., Perinatal Research Center, University of Alberta, Edmonton, AB T6G-2S2, Canada. E-mail: jocelynnc{at}hotmail.com

Myometrial contractions of labor result from an increase in myometrial activation and stimulation. Activation develops through the expression of contraction associated proteins (CAPs), including oxytocin receptors (OTR), connexin-43 (Cx-43), and prostaglandin F₂ receptors (FP). Stimulation involves increases in contractile agonists including prostaglandin E₂ (PGE₂) and prostaglandin F₂ (PGF₂) that may result from increases in prostaglandin endoperoxide H synthase (PGHS)-2. A mouse model of preterm birth was used to study gene expression involved in myometrial activation and stimulation. To induce preterm birth, pregnant C57BL/6J mice were intubated with 6 g/kg ethanol on gestational day 16 and were killed every 6 h from treatment until birth. RIA was used to measure uterine PGE₂ and PGF₂, while PGHS-2, OTR, Cx-43, and FP messenger RNA levels were measured by ribonuclease protection assay. Increases in CAP mRNA were associated with term and preterm birth. There were differences in stimulation effectors associated with preterm and term birth. Uterine PGF₂ values were increased only at the time of term birth, but PGE₂ was elevated during both preterm and term labor. These data suggest that existing levels of PGF₂ are sufficient for preterm birth when CAP expression is increased, but term labor requires increases in PGE₂, PGF₂, and CAPs. The PGHS-2 messenger RNA expression pattern suggests that it is a CAP.

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