| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Unité d'Endocrinologie et Métabolisme, University of Louvain Faculty of Medicine, Brussels, Belgium
2 Diabetes Research Center, Vrije Universiteit, Brussels, Belgium
The contribution of Ca2+ release from intracellular stores to the rise in the free cytosolic Ca2+ concentration ([Ca2+]c) triggered by Ca2+ influx was investigated in mouse pancreatic ß-cells. Depolarization of ß-cells by 45 mM K+ (in the presence of 15 mM glucose and 0.1 mM diazoxide) evoked two types of [Ca2+]c responses: a monotonic and sustained elevation; or a sustained elevation superimposed by a transient [Ca2+]c peak (TCP) (40–120 s after the onset of depolarization). Simultaneous measurements of [Ca2+]c and voltage-dependent Ca2+ current established that the TCP did not result from a larger Ca2+ current. Abolition of the TCP by thapsigargin and its absence in sarco-endoplasmic reticulum Ca2+-ATPase 3 (SERCA3) knockout mice show that it is caused by Ca2+ mobilization from the endoplasmic reticulum. A TCP could not be evoked by the sole depolarization of ß-cells but required a rise in [Ca2+]c pointing to a Ca2+-induced Ca2+ release (CICR). This CICR did not involve inositol 1,4,5-trisphosphate (IP3) receptors (IP3Rs) 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 mimicked by caffeine, a RyR agonist. Moreover, RyR1 and RyR2 mRNA were not found and RyR3 mRNA was only slightly expressed in purified ß-cells. A CICR could also be detected in a limited number of cells in response to glucose. Our data demonstrate, for the first time in living cells, the existence of an atypical CICR that is independent from the IP3R and the RyR. This CICR is prominent in response to a supraphysiological stimulation with high K+, but plays little role in response to glucose in non-obese mouse pancreatic ß-cells.
(Received 30 April 2004;
accepted after revision 21 June 2004;
first published online 24 June 2004)
Corresponding author P. Gilon: Unité d'Endocrinologie et Métabolisme, University of Louvain Faculty of Medicine, Brussels, Belgium. Email: gilon{at}endo.ucl.ac.be
This article has been cited by other articles:
|
|
 |
|
  V. Dror, T. B. Kalynyak, Y. Bychkivska, M. H. Z. Frey, M. Tee, K. D. Jeffrey, V. Nguyen, D. S. Luciani, and J. D. Johnson Glucose and Endoplasmic Reticulum Calcium Channels Regulate HIF-1{beta} via Presenilin in Pancreatic {beta}-Cells J. Biol. Chem., April 11, 2008; 283(15): 9909 - 9916. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. S. Nunemaker, R. Bertram, A. Sherman, K. Tsaneva-Atanasova, C. R. Daniel, and L. S. Satin Glucose Modulates [Ca2+]i Oscillations in Pancreatic Islets via Ionic and Glycolytic Mechanisms Biophys. J., September 15, 2006; 91(6): 2082 - 2096. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Hughes, A. K. Lee, and A. Tse Dominant Role of Sarcoendoplasmic Reticulum Ca2+-ATPase Pump in Ca2+ Homeostasis and Exocytosis in Rat Pancreatic {beta}-Cells Endocrinology, March 1, 2006; 147(3): 1396 - 1407. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Nadif Kasri, G. Bultynck, J. B. Parys, G. Callewaert, L. Missiaen, and H. De Smedt Suramin and Disulfonated Stilbene Derivatives Stimulate the Ca2+-Induced Ca2+-Release Mechanism in A7r5 Cells Mol. Pharmacol., July 1, 2005; 68(1): 241 - 250. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Kang, O. G Chepurny, M. J Rindler, L. Collis, Z. Chepurny, W.-h. Li, M. Harbeck, M. W Roe, and G. G Holz A cAMP and Ca2+ coincidence detector in support of Ca2+-induced Ca2+ release in mouse pancreatic {beta} cells J. Physiol., July 1, 2005; 566(1): 173 - 188. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Bertram and A. Sherman Filtering of Calcium Transients by the Endoplasmic Reticulum in Pancreatic {beta}-Cells Biophys. J., December 1, 2004; 87(6): 3775 - 3785. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
O. Dyachok and E. Gylfe Ca2+-induced Ca2+ Release via Inositol 1,4,5-trisphosphate Receptors Is Amplified by Protein Kinase A and Triggers Exocytosis in Pancreatic {beta}-Cells J. Biol. Chem., October 29, 2004; 279(44): 45455 - 45461. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
