Stimulation of platelet-activating factor (PAF) receptors increases inositol phosphate production and cytosolic free Ca2+ concentrations in N1E-115 neuroblastoma cells
Autor: | M. Ziade, Jean Verdetti, M. Diserbo, F. Cand |
---|---|
Rok vydání: | 1995 |
Předmět: |
medicine.medical_specialty
Indoles Time Factors Physiology Inositol Phosphates Stimulation Receptors Cell Surface Calcium-Transporting ATPases Platelet Membrane Glycoproteins Biology Phosphatidylinositols Receptors G-Protein-Coupled chemistry.chemical_compound Mice Neuroblastoma Mediator Cytosol Nifedipine Lanthanum Internal medicine medicine Tumor Cells Cultured Animals Platelet Activating Factor Inositol phosphate Molecular Biology chemistry.chemical_classification Manganese Platelet-activating factor Terpenes Depolarization Cell Biology respiratory system Phosphate Culture Media Endocrinology chemistry Biophysics Carcinogens Thapsigargin lipids (amino acids peptides and proteins) Calcium Calcium Channels medicine.drug |
Zdroj: | Cell calcium. 17(6) |
ISSN: | 0143-4160 |
Popis: | Platelet-activating factor (1-O-alkyl-2-acetyl- sn -glycero-3-phosphorylcholine, PAF) has recently been recognized as an important mediator in the pathophysiology of brain injury. This study demonstrates that, in suspended populations of N1E-115 cells loaded with Indo-1, biologically relevant concentrations of PAF produce a rapid and transient elevation in cytosolic free calcium concentration ([Ca 2+ ] i ). Moreover, nanomolar concentrations of PAF increase [ 3 H]-inositol phosphate production. Using lyso-PAF and the specific PAF-receptor antagonists BN52021 and BN50739, we show that these effects were mediated by stimulation of PAF receptors. Experiments performed in Ca 2+ free medium show that PAF-induced [Ca 2+ ] i increase is the result of an influx of Ca 2+ and of the release of intracellular Ca 2+ stores. Studies of Mn 2+ influx argue in favour of additional pathways for the PAF-induced Ca 2+ influx other than the pathway for the thapsigargin-induced Ca 2+ influx. Using the whole-cell voltage-clamp technique, we observe that PAF induces an increase of Ltype Ca 2+ current. However, the effects of La 3+ , nifedipine and KCI-induced depolarization on the PAF-induced [Ca 2+ ] i increase suggest a minor participation of these voltage-gated Ca 2+ channels in the response to PAR Altogether the results point to the existence of a PAF-induced Ca 2+ influx through receptor-operated Ca 2+ permeant channels. |
Databáze: | OpenAIRE |
Externí odkaz: |