Atypical Ca2+-induced Ca2+ release from a sarco-endoplasmic reticulum Ca2+-ATPase 3-dependent Ca2+ pool in mouse pancreatic beta-cells

The Journal of Physiology
Melanie C BeauvoisP Gilon

Abstract

The contribution of Ca(2+) release from intracellular stores to the rise in the free cytosolic Ca(2+) concentration ([Ca(2+)](c)) triggered by Ca(2+) influx was investigated in mouse pancreatic beta-cells. Depolarization of beta-cells by 45 mm K(+) (in the presence of 15 mm glucose and 0.1 mm diazoxide) evoked two types of [Ca(2+)](c) responses: a monotonic and sustained elevation; or a sustained elevation superimposed by a transient [Ca(2+)](c) peak (TCP) (40-120 s after the onset of depolarization). Simultaneous measurements of [Ca(2+)](c) and voltage-dependent Ca(2+) current established that the TCP did not result from a larger Ca(2+) current. Abolition of the TCP by thapsigargin and its absence in sarco-endoplasmic reticulum Ca(2+)-ATPase 3 (SERCA3) knockout mice show that it is caused by Ca(2+) mobilization from the endoplasmic reticulum. A TCP could not be evoked by the sole depolarization of beta-cells but required a rise in [Ca(2+)](c) pointing to a Ca(2+)-induced Ca(2+) release (CICR). This CICR did not involve inositol 1,4,5-trisphosphate (IP(3)) receptors (IP(3)Rs) because it was resistant to heparin. Nor did it involve ryanodine receptors (RyRs) because it persisted after blockade of RyRs with ryanodine, and was not...Continue Reading

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Citations

Sep 23, 2014·Cell Calcium·Patrick GilonMagalie A Ravier
Feb 10, 2017·Cell Calcium·Daniel Leon-AparicioAgustin Guerrero-Hernandez
Jul 4, 2006·Biophysical Journal·Craig S NunemakerLeslie S Satin
Nov 14, 2018·The Journal of Biological Chemistry·Wataru R YamamotoCarmella Evans-Molina
Jan 5, 2008·The Journal of Biological Chemistry·Vardit DrorJames D Johnson
Feb 20, 2009·American Journal of Physiology. Cell Physiology·P Charukeshi ChandrasekeraJonathan Lytton
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