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TRPM4 impacts on Ca 2+ signals during agonist-induced insulin secretion in pancreatic β-cells

TRPM4 impacts on Ca 2+ signals during agonist-induced insulin secretion in pancreatic β-cells,10.1016/j.mce.2008.11.011,Molecular and Cellular Endocri

TRPM4 impacts on Ca 2+ signals during agonist-induced insulin secretion in pancreatic β-cells   (Citations: 5)
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TRPM4 is a Ca2+-activated non-selective cation (CAN) channel that functions in cell depolarization, which is important for Ca2+ influx and insulin secretion in pancreatic β-cells. We investigated TRPM4 expression and function in the β-cell lines HIT-T15 (hamster), RINm5F (rat), β-TC3 (mouse), MIN-6 (mouse) and the α-cell line INR1G9 (hamster). By RT-PCR, we identified TRPM4 transcripts in α- and β-cells. Patch-clamp recordings with increasing Ca2+ concentrations resulted in a dose-dependent activation of TRPM4 with the greatest depolarizing currents recorded from hamster-derived cells. Further, Ca2+ imaging experiments revealed that inhibition of TRPM4 by a dominant-negative effect significantly decreased the magnitude of the Ca2+ signals generated by agonist stimulation compared to control cells. The decrease in the [Ca2+]i resulted in reduced insulin secretion. Our data suggest that depolarizing currents generated by TRPM4 are an important component in the control of intracellular Ca2+ signals necessary for insulin secretion and perhaps glucagon from α-cells.
Journal: Molecular and Cellular Endocrinology - MOL CELL ENDOCRINOL , vol. 299, no. 2, pp. 194-203, 2009
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