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Hydrogen peroxide activates agonist-sensitive Ca(2+)-flux pathways in canine venous endothelial cells
T N Doan1, D L Gentry, A A Taylor
1Department of Pediatrics, Baylor College of Medicine, Houston, TX 77030.
The Biochemical Journal
|January 1, 1994
Summary
Hydrogen peroxide (H2O2) activates calcium (Ca2+) signaling in endothelial cells by releasing Ca2+ from internal stores and promoting Ca2+ influx. This suggests H2O2 may function as an intercellular messenger.
Area of Science:
- Cellular Biology
- Physiology
- Biochemistry
Background:
- Purinergic receptors mediate cellular responses.
- Calcium (Ca2+) signaling is crucial for cell function.
- Hydrogen peroxide (H2O2) is a biological oxidant with signaling roles.
Purpose of the Study:
- To investigate the effect of H2O2 on purinergic-receptor-stimulated Ca2+ signaling in canine venous endothelial cells.
- To elucidate the mechanisms by which H2O2 influences intracellular Ca2+ levels.
Main Methods:
- Measurement of cytosolic free Ca2+ ([Ca2+]i) in response to H2O2.
- Characterization of H2O2-sensitive intracellular Ca2+ pools using sequential stimulation with H2O2, ionomycin, and ATP.
- Assessment of H2O2-induced Ca2+ release using thapsigargin, an inhibitor of the Ca2+ pump.
- Evaluation of H2O2-stimulated Ca2+ influx using inhibitors like Ni2+, La3+, and SKF-96365.
Main Results:
- H2O2 dose-dependently increased [Ca2+]i.
- H2O2-induced Ca2+ release originated from internal stores, specifically the inositol trisphosphate-sensitive Ca2+ pool.
- H2O2-stimulated Ca2+ influx occurred via the agonist-sensitive Ca2+ influx pathway.
- H2O2 pretreatment diminished subsequent ATP-induced Ca2+ release.
Conclusions:
- H2O2 acts as an intercellular messenger, modulating Ca2+ signaling in endothelial cells.
- H2O2 stimulates Ca2+ release from internal stores and promotes Ca2+ influx.
- These findings highlight a novel signaling role for H2O2 in endothelial cell communication.