TRPM7 activation potentiates SOCE in enamel cells but requires ORAI.

Cell Calcium
Guilherme H Souza BomfimRodrigo S Lacruz

Abstract

Calcium (Ca2+) release-activated Ca2+ (CRAC) channels mediated by STIM1/2 and ORAI (ORAI1-3) proteins form the dominant store-operated Ca2+ entry (SOCE) pathway in a wide variety of cells. Among these, the enamel-forming cells known as ameloblasts rely on CRAC channel function to enable Ca2+ influx, which is important for enamel mineralization. This key role of the CRAC channel is supported by human mutations and animal models lacking STIM1 and ORAI1, which results in enamel defects and hypomineralization. A number of recent reports have highlighted the role of the chanzyme TRPM7 (transient receptor potential melastanin 7), a transmembrane protein containing an ion channel permeable to divalent cations (Mg2+, Ca2+), as a modulator of SOCE. This raises the question as to whether TRPM7 should be considered an alternative route for Ca2+ influx, or if TRPM7 modifies CRAC channel activity in enamel cells. To address these questions, we monitored Ca2+ influx mediated by SOCE using the pharmacological TRPM7 activator naltriben and the inhibitor NS8593 in rat primary enamel cells and in the murine ameloblast cell line LS8 cells stimulated with thapsigargin. We also measured Ca2+ dynamics in ORAI1/2-deficient (shOrai1/2) LS8 cells and i...Continue Reading

Citations

Sep 27, 2020·International Journal of Molecular Sciences·Vladimir Chubanov, Thomas Gudermann
Jan 5, 2021·Frontiers in Cellular Neuroscience·Ashwini HariharanThomas A Longden
May 1, 2021·International Journal of Molecular Sciences·Kristóf KádárÁkos Zsembery
Aug 31, 2021·Frontiers in Endocrinology·Veronica CostinitiRodrigo S Lacruz

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