Bradykinin-activated contractile signalling pathways in human myometrial cells are differentially regulated by arrestin proteins

Molecular and Cellular Endocrinology
Jonathon M WilletsJustin C Konje

Abstract

Bradykinin is associated with infections and inflammation, which given the strong correlation between uterine infection and preterm labour may imply that it could play a role in this process. Therefore, we investigated bradykinin signalling, and the roles that arrestin proteins play in their regulation in human myometrial cells. Bradykinin induced rapid, transient intracellular Ca(2+) increases that were inhibited following B2 receptor (B2R) antagonism. Arrestin2 or arrestin3 depletion enhanced and prolonged bradykinin-stimulated Ca(2+) responses, and attenuated B2R desensitisation. Knockdown of either arrestin enhanced B2R-stimulated ERK1/2 signals. Moreover, depletion of either arrestin elevated peak-phase p38-MAPK signalling, yet only arrestin3 depletion prolonged B2R-induced p38-MAPK signals. Arrestin2-knockdown augmented bradykinin-induced cell movement. Bradykinin stimulates pro-contractile signalling mechanisms in human myometrial cells and arrestin proteins play key roles in their regulation. Our data suggest bradykinin not only acts as an utertonin, but may also have the potential to enhance the contractile environment of the uterus.

References

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Citations

Mar 16, 2016·Women's Health·Aleena Banerji, Marc Riedl
Oct 17, 2015·Trends in Endocrinology and Metabolism : TEM·Ashish SrivastavaArun K Shukla
Sep 5, 2018·American Journal of Reproductive Immunology : AJRI·Samantha Sheller-MillerRamkumar Menon
Aug 13, 2021·European Journal of Obstetrics & Gynecology and Reproductive Biology: X·Susanne HesselmanAnna Sandström
Aug 17, 2021·Frontiers in Pharmacology·Chaolu ChenDanqing Chen

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