Enhanced Uterine Contractility and Stillbirth in Mice Lacking G Protein-Coupled Receptor Kinase 6 (GRK6): Implications for Oxytocin Receptor Desensitization

Feb 18, 2016Molecular endocrinology (Baltimore, Md.)

Increased Uterine Contractions and Stillbirth in Mice Missing GRK6, Affecting Oxytocin Receptor Response

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Abstract

Mice lacking GRK6 exhibit enhanced uterine contractility during labor.

  • Uterine levels of GRK6 increase during pregnancy.
  • Mice without GRK6 show greater uterine contractility during both spontaneous and oxytocin-induced labor compared to wild-type and GRK5 knockout mice.
  • Enhanced contractility in GRK6-deficient mice is associated with higher rates of term stillbirth.
  • Recruitment of a protein called β-arrestin to the oxytocin receptor, which is important for receptor desensitization, relies on GRK6.
  • GRK6-mediated desensitization of the oxytocin receptor may be necessary for normal uterine contractions and healthy fetal outcomes.

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