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Ca2+ entry induced by cyclic ADP-ribose in intact T-lymphocytes
A H Guse1, I Berg, C P da Silva
1University of Hamburg, Institute of Physiological Chemistry, Department of Enzyme Chemistry, Grindelallee 117, D-20146 Hamburg, Germany. guse@uke.uni-hamburg.de
The Journal of Biological Chemistry
|March 28, 1997
Summary
Cyclic ADP-ribose (cADPr) triggers calcium spikes in T-lymphocytes, dependent on extracellular calcium. This suggests cADPr plays a role in calcium entry into these immune cells.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- Cyclic ADP-ribose (cADPr) is a known Ca2+-mobilizing second messenger.
- Previous studies showed cADPr releases Ca2+ from intracellular stores in permeabilized T-lymphocytes.
Purpose of the Study:
- To investigate the role of cADPr in Ca2+ signaling in intact T-lymphocytes.
- To elucidate the mechanism of cADPr-induced Ca2+ release and entry.
Main Methods:
- Microinjection of cADPr into single T-lymphocytes.
- Ratiometric digital Ca2+ imaging.
- Use of specific antagonists (8-NH2-cADPr) and inhibitors (Zn2+, SK-F 96365).
Main Results:
- Microinjected cADPr induced dose-dependent, repetitive Ca2+ spikes in T-lymphocytes.
- These Ca2+ spikes were largely dependent on extracellular Ca2+.
- Ca2+ spike initiation occurred at plasma membrane "hot spots" and propagated intracellularly.
- Inhibition studies confirmed the role of extracellular Ca2+ and specific signaling pathways.
Conclusions:
- cADPr induces Ca2+ entry into intact T-lymphocytes.
- The findings suggest a novel role for cADPr in regulating Ca2+ influx in T-cells.
- This mechanism may be crucial for T-lymphocyte activation and function.