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Trifluoperazine Attenuates Store-Dependent Ca2+ Entry in Macrophages
Z I Krutetskaya1, L S Milenina2, A A Naumova2
1St. Petersburg State University, St. Petersburg, 199034, Russia. z.krutetskaya@spbu.ru.
Doklady. Biochemistry and Biophysics
|March 15, 2018
Summary
Neuroleptic trifluoperazine inhibits calcium (Ca2+) entry in rat macrophages. This suggests calsequestrin plays a role in regulating calcium entry, a key process in macrophage function.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- Macrophages are crucial immune cells involved in various physiological and pathological processes.
- Calcium signaling is essential for macrophage activation and function.
- Endoplasmic reticulum calcium stores play a significant role in regulating intracellular calcium levels.
Purpose of the Study:
- To investigate the role of calsequestrin in store-dependent calcium (Ca2+) entry in rat peritoneal macrophages.
- To determine if inhibiting calsequestrin affects calcium influx induced by endoplasmic reticulum calcium-ATPase inhibitors.
Main Methods:
- Fura-2AM microfluorimetry was used to measure intracellular calcium concentrations.
- Rat peritoneal macrophages were preincubated with trifluoperazine, a calsequestrin inhibitor.
- Calcium entry was induced using thapsigargin or cyclopiazonic acid, inhibitors of endoplasmic reticulum Ca2+-ATPase.
Main Results:
- Preincubation with trifluoperazine significantly inhibited store-dependent calcium (Ca2+) entry.
- This inhibition was observed when calcium entry was induced by both thapsigargin and cyclopiazonic acid.
- The findings demonstrate a direct effect of calsequestrin inhibition on calcium influx.
Conclusions:
- Calsequestrin is involved in the regulation of store-dependent calcium (Ca2+) entry in macrophages.
- Inhibiting calsequestrin with trifluoperazine effectively blocks calcium influx.
- These results provide new insights into the mechanisms controlling calcium homeostasis in macrophages.
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