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Ca2+ release from inositol trisphosphate-sensitive stores is not modulated by intraluminal [Ca2+]
1Department of Physiology, University of Rochester School of Medicine and Dentistry, New York 14642.
The Journal of Biological Chemistry
|February 25, 1992
Summary
A model proposed that intraluminal calcium influences inositol 1,4,5-trisphosphate (Ins(1,4,5)P3)-induced calcium release. Experiments in exocrine cells did not support this model, as predicted effects on calcium release sensitivity and decay were not observed.
Area of Science:
- Cell Biology
- Biochemistry
- Physiology
Background:
- A model suggested intraluminal calcium modulates inositol 1,4,5-trisphosphate (Ins(1,4,5)P3)-induced calcium release.
- This modulation was proposed to occur via the Ins(1,4,5)P3 receptor/Ca2+ channel complex.
Purpose of the Study:
- To test the predictions of a model proposing intraluminal calcium modulation of Ins(1,4,5)P3-induced Ca2+ release.
- To investigate the effects of intraluminal Ca2+ on Ins(1,4,5)P3 receptor sensitivity and passive Ca2+ store depletion.
Main Methods:
- Measurements of Ins(1,4,5)P3-induced Ca2+ release in permeabilized exocrine cells.
- Analysis of passive Ca2+ loss from stores after inhibition of the Ca2+ pump using thapsigargin.
Main Results:
- Neither the predicted effect of intraluminal Ca2+ on Ins(1,4,5)P3-induced Ca2+ release sensitivity nor non-exponential passive Ca2+ decay was observed.
- Experimental findings contradicted key predictions of the proposed model.
Conclusions:
- The proposed model for intraluminal calcium modulation of Ins(1,4,5)P3-induced Ca2+ release is not supported by experimental evidence in this model system.
- Further research is needed to understand the regulation of intracellular calcium release mechanisms.