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Lithium opens store-operated channels in human platelets.
1Centro de Investigaciones Cardiovasculares, Universidad Nacional de La Plata, 60 Y 120, La Plata, 1900, Argentina. Cicme@atlas.med.unlp.edu.ar
Biochemical and Biophysical Research Communications
|January 13, 2000
Summary
Lithium preincubation in platelets increases basal manganese influx, suggesting it opens store-operated calcium channels. This explains why further store depletion doesn't increase influx in lithium-treated cells.
Area of Science:
- Cell Biology
- Biochemistry
- Physiology
Background:
- Calcium (Ca2+) release from internal stores is linked to extracellular Ca2+ influx.
- Platelets play a crucial role in hemostasis and thrombosis, involving calcium signaling.
Purpose of the Study:
- To investigate the effect of lithium on calcium (Ca2+) influx in platelets.
- To determine if lithium influences store-operated calcium channels.
Main Methods:
- Measurement of intracellular calcium concentration using Fura2 fluorescence.
- Assessing manganese (Mn2+) influx as a surrogate for Ca2+ influx.
- Utilizing thapsigargin to deplete internal calcium stores.
Main Results:
- Platelets preincubated in lithium showed higher basal Mn2+ influx compared to those in sodium.
- Agonist-stimulated Mn2+ influx was lower in lithium-preincubated platelets.
- Lithium preincubation led to basal Mn2+ entry without further increase upon store depletion by thapsigargin, unlike sodium or N-methyl glucamine.
Conclusions:
- Lithium induces calcium influx through store-operated channels in platelets.
- This mechanism explains the observed lack of additivity between basal and store-depletion-triggered influx in lithium-treated cells.