ArticleAmerican journal of physiology. Endocrinology and metabolism2011
β-Arrestin mediates oxytocin receptor signaling, which regulates uterine contractility and cellular migration.
Article in American journal of physiology. Endocrinology and metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 41 citations in OpenAlex.
- Association between oxytocin exposure in the second stage of labor and postpartum hemorrhage among nulliparous patients with neuraxial analgesia.Pregnancy (Hoboken, N.J.) · 2026Article
- Risk of postpartum hemorrhage with increasing first stage labor duration.Scientific reports · 2024Article
- Oxytocin accelerates tight junction formation and impairs cellular migration in 3D spheroids: evidence from Gapmer-induced exon skipping.Frontiers in cellular neuroscience · 2022Article
- Oxytocin and secretin receptors - implications for dry eye syndrome and ocular pain.Frontiers in ophthalmology · 2022Review
- Naturally Occurring Genetic Variants in the Oxytocin Receptor Alter Receptor Signaling Profiles.ACS pharmacology & translational science · 2021Article
- Review
- Oxytocin antagonism prevents pregnancy-associated aortic dissection in a mouse model of Marfan syndrome.Science translational medicine · 2019Article
- β-arrestin 1 regulates β2-adrenergic receptor-mediated skeletal muscle hypertrophy and contractility.Skeletal muscle · 2018Article
- Article
- The Oxytocin Product Correlates with Total Oxytocin Received during Labor: A Research Methods Study.American journal of perinatology · 2018Article
- The association of single-nucleotide polymorphisms in the oxytocin receptor and G protein-coupled receptor kinase 6 (GRK6) genes with oxytocin dosing requirements and labor outcomes.American journal of obstetrics and gynecology · 2017Article
- Enhanced Uterine Contractility and Stillbirth in Mice Lacking G Protein-Coupled Receptor Kinase 6 (GRK6): Implications for Oxytocin Receptor Desensitization.Molecular endocrinology (Baltimore, Md.) · 2016Article
- G Protein-coupled Receptor Biased Agonism.Journal of cardiovascular pharmacology · 2016Review
- Progesterone Metabolites Produced by Cytochrome P450 3A Modulate Uterine Contractility in a Murine Model.Reproductive sciences (Thousand Oaks, Calif.) · 2015Article
- Minireview: Spatial Programming of G Protein-Coupled Receptor Activity: Decoding Signaling in Health and Disease.Molecular endocrinology (Baltimore, Md.) · 2015Review
- Salt restriction leads to activation of adult renal mesenchymal stromal cell-like cells via prostaglandin E2 and E-prostanoid receptor 4.Hypertension (Dallas, Tex. : 1979) · 2015Article
- Osteoblast regulation via ligand-activated nuclear trafficking of the oxytocin receptor.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- The influence of maternal body mass index on myometrial oxytocin receptor expression in pregnancy.Reproductive sciences (Thousand Oaks, Calif.) · 2013Article
- Review
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Desensitization of the oxytocin receptor (OXTR) in the setting of prolonged oxytocin exposure may lead to dysfunctional labor, which increases the risk for cesarean delivery, and uterine atony, which may result in postpartum hemorrhage. The molecular mechanism for OXTR desensitization is through the agonist-mediated recruitment of the multifunctional protein β-arrestin. In addition to its desensitizing function, β-arrestins have recently been shown to simultaneously activate downstream signaling. We tested whether oxytocin stimulation promotes β-arrestin-mediated OXTR desensitization in vivo and activates β-arrestin-mediated mitogen-activated protein kinase (MAPK) growth signaling. Uterine muscle strips isolated from wild-type mice exhibited diminished uterine contractility following repeated exposure to oxytocin, whereas uterine muscle strips from β-arrestin-1 and β-arrestin-2 knockout mice showed no desensitization. Utilizing siRNA knockdown of β-arrestin-1 and β-arrestin-2 in HEK-293 cells expressing the OXTR, we demonstrated oxytocin-mediated MAPK signaling that was dependent on β-arrestin-1 and β-arrestin-2. Wild-type and β-arrestin-1 and β-arrestin-2 knockout mice receiving intravenous oxytocin also demonstrated oxytocin-mediated MAPK signaling that was dependent on β-arrestin-1 and β-arrestin-2. Finally, to test the significance of β-arrestin-mediated signaling from the OXTR, HEK-293 cells expressing the OXTR showed β-arrestin-dependent proliferation in a cell migration assay following oxytocin treatment. In conclusion, β-arrestin is a multifunctional scaffold protein that mediates both desensitization of the OXTR, leading to decreases in uterine contractility, and MAPK growth signaling following stimulation by oxytocin. The development of unique OXTR ligands that prevent receptor desensitization may be a novel approach in the treatment of adverse clinical events secondary to prolonged oxytocin therapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.