|
|
||||||||
-cells communicate via intermittent release of ATP
Department of Medical Cell Biology, University of Uppsala, SE-751 23 Uppsala, Sweden
Submitted 7 October 2003 ; accepted in final form 6 January 2004
The role of external ATP for intercellular communication was studied in glucose-stimulated pancreatic
-cells isolated from ob/ob mice. Digital image analyses with fura-2 revealed spontaneous transients of cytoplasmic Ca2+ appearing in synchrony in the absence of cell contacts. After removal of slow oscillations with methoxyverapamil, addition of ATP (0.1100 µM) resulted in prompt firing of a transient, followed by suppression of the generation and synchronization of spontaneously occurring transients. It was possible to trigger transients during the suppressive phase by raising the concentration of ATP. The dual action of ATP was mimicked by ADP or 2-methylthio-ATP but not by AMP or UTP. The number of spontaneous transients and their synchronization were reduced in the presence of the dephosphorylating agent apyrase. Additional evidence that intermittent release of ATP participates in the generation of spontaneous Ca2+ transients was obtained from the suppression observed from use of antagonists of the purinoceptors [suramin (0.330 µM), pyridoxalphosphate-6-azophenyl-2,4-disulfonic acid (PPADS; 1030 µM) and 2-deoxy-N-methyladenosine (MRS 2179; 0.330 µM)] or from counteracting
-cell release of ATP by inhibiting exocytosis with 100 nM epinephrine, 100 nM somatostatin, or lowering the temperature below 30°C. The data indicate that ATP has time-dependent actions (prompt stimulation followed by inhibition) on the generation of Ca2+ transients mediated by P2Y receptors. It is proposed that
-cells both receive a neural ATP signal with coordinating effects on their Ca2+ oscillations and propagate this message to adjacent cells via intermittent release of ATP combined with gap junction coupling.
calcium oscillations; calcium transients; purinoceptors; synchronization
This article has been cited by other articles:
![]() |
E. Tuduri, E. Filiputti, E. M. Carneiro, and I. Quesada Inhibition of Ca2+ signaling and glucagon secretion in mouse pancreatic {alpha}-cells by extracellular ATP and purinergic receptors Am J Physiol Endocrinol Metab, May 1, 2008; 294(5): E952 - E960. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Brissova, A. Shostak, M. Shiota, P. O. Wiebe, G. Poffenberger, J. Kantz, Z. Chen, C. Carr, W. G. Jerome, J. Chen, et al. Pancreatic Islet Production of Vascular Endothelial Growth Factor-A Is Essential for Islet Vascularization, Revascularization, and Function Diabetes, November 1, 2006; 55(11): 2974 - 2985. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Nilsson, L. M. Nilsson, Y.-W. Chen, J. D. Molkentin, D. Erlinge, and M. F. Gomez High Glucose Activates Nuclear Factor of Activated T Cells in Native Vascular Smooth Muscle Arterioscler. Thromb. Vasc. Biol., April 1, 2006; 26(4): 794 - 800. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. Onfelt, M. A. Purbhoo, S. Nedvetzki, S. Sowinski, and D. M. Davis Long-Distance Calls Between Cells Connected by Tunneling Nanotubules Sci. Signal., December 6, 2005; 2005(313): pe55 - pe55. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Salehi, S. S. Qader, E. Grapengiesser, and B. Hellman Inhibition of Purinoceptors Amplifies Glucose-Stimulated Insulin Release With Removal of its Pulsatility Diabetes, July 1, 2005; 54(7): 2126 - 2131. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |