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Thapsigargin-induced Ca2+ release from sarcoplasmic reticulum and asolectin vesicles
1Department of Physics, Portland State University, Oregon.
Cell Calcium
|February 1, 1994
Summary
Thapsigargin causes calcium release from cell stores by acting as an ionophore, not just by inhibiting Ca(2+)-ATPase activity. This ionophoric effect on lipid membranes explains calcium release at higher concentrations.
Area of Science:
- Biochemistry
- Cell Biology
- Membrane Biophysics
Background:
- Thapsigargin is known to inhibit Ca(2+)-ATPase, increasing cytosolic calcium.
- The mechanism of calcium release by thapsigargin has been attributed to ATPase inhibition.
Purpose of the Study:
- To investigate the mechanism of calcium release induced by thapsigargin.
- To determine if thapsigargin has effects beyond Ca(2+)-ATPase inhibition.
Main Methods:
- Studied thapsigargin's effect on sarcoplasmic reticulum vesicles.
- Examined thapsigargin's impact on calcium-loaded asolectin liposomes (protein-free model).
Main Results:
- Thapsigargin induced rapid calcium release from sarcoplasmic reticulum vesicles at higher concentrations.
- Thapsigargin also caused concentration-dependent calcium release in protein-free liposomes.
- These effects suggest an ionophoric mechanism independent of ATPase inhibition.
Conclusions:
- Micromolar concentrations of thapsigargin induce calcium release via an ionophoric effect on lipid membranes.
- This ionophoric activity is distinct from its inhibition of Ca(2+)-ATPase activity.