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

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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