Molecular pathways regulating contractility in rat uterus through late gestation and parturition - 20/06/12
Résumé |
Objective |
Endogenous uterine agonists can activate numerous signaling pathways to effect increased force. Our objective was to assess expression of key constituents of these pathways, in alliance with contractile function, through late gestation and during term and preterm labor.
Study Design |
Using myography, we measured the response to 3 agonists compared with depolarization alone (K+, 124 mEq/L) and calculated agonist/depolarization ratio. We measured gene expression using quantitative reverse transcription–polymerase chain reaction.
Results |
Contractile responsiveness to depolarization alone, oxytocin, or endothelin-1 increased during pregnancy compared with nonpregnant animals. The agonist/depolarization ratio did not change during uterine activation or parturition. Inhibition of rhoA-associated kinase decreased responses to oxytocin in all tissues, but significantly more during uterine activation. Expression of rhoA and rhoA-associated kinase was increased significantly in active labor at term or preterm.
Conclusion |
The rhoA/rhoA-associated kinase pathway is a key regulator of uterine activation during labor and may be a useful target for the prevention of spontaneous preterm birth.
Le texte complet de cet article est disponible en PDF.Key words : parturition, progesterone, rhoA, rhoA-associated kinase, uterine activation
Plan
| Supported by grants from the Canadian Institutes for Health Research (Operating grant [B.F.M.]; strategic training grant [P.L.A.]), the University of Alberta Perinatal Research Centre (P.L.A.) and the Alberta Heritage Foundation for Medical Research (Equipment grant [B.F.M.]). |
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| The authors report no conflict of interest. |
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| Reprints not available from the authors. |
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| Cite this article as: Taggart MJ, Arthur P, Zielnik B, et al. Molecular pathways regulating contractility in rat uterus through late gestation and parturition. Am J Obstet Gynecol 2012;207:76.e15-24. |
Vol 207 - N° 1
P. 76.e15-76.e24 - juillet 2012 Retour au numéro
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