title: Effect of heat shock on intracellular calcium mobilization in neuroblastoma x glioma hybrid cells.
abstract: The effect of heat shock on agonist-stimulated intracellular Ca2+ mobilization and the expression of heat shock protein 72 (hsp72) in neuroblastoma x glioma hybrid cells (NG 108-15 cells) were examined. Hsp72 was expressed at 6 h after heat shock (42.5 degrees C, 2 h), reached a maximum at 12 h, and decreased thereafter. Bradykinin-induced [Ca2+]i rise was attenuated to 28% of control by heat shock at 2 h after heat shock, and reversion to the control level was seen 12 h later. When the cells were treated with quercetin or antisense oligodeoxyribonucleotide against hsp72 cDNA, the synthesis of hsp72 was not induced by heat shock, whereas bradykinin-induced [Ca2+]i rise was abolished and the [Ca2+]i rise was not restored. Recovery from this stressed condition was evident when cells were stimulated by the Ca(2+)-ATPase inhibitor thapsigargin, even in the presence of either quercetin or antisense oligodeoxyribonucleotide. Inositol 1,4,5-trisphosphate (IP3) production was not altered by heat shock at 12 h after heat shock, whereas IP3 receptor binding activity was reduced to 45.3%. In the presence of quercetin or antisense oligodeoxyribonucleotide, IP3 receptor binding activity decreased and reached 27.2% of the control 12 h after heat shock. Our working thesis is that heat shock transiently suppresses the IP3-mediated intracellular Ca2+ signal transduction system and that hsp72 is involved in the recovery of bradykinin-induced [Ca2+]i rise.
authors.affiliation: Department of Pharmacology, Kobe University School of Medicine, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Katayama
authors.forename: H
authors.initials: H
authors.lastname: Shuntoh
authors.forename: S
authors.initials: S
authors.lastname: Matsuyama
authors.forename: C
authors.initials: C
authors.lastname: Tanaka
mesh_terms: D000818:Animals; D001692:Biological Transport; D001920:Bradykinin / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000378:metabolism; D005910:Glioma / Q000378:metabolism* / Q000473:pathology; D006360:Heat-Shock Proteins / Q000378:metabolism*; D006358:Hot Temperature; D006822:Hybrid Cells / Q000378:metabolism; D015544:Inositol 1,4,5-Trisphosphate / Q000096:biosynthesis; D053496:Inositol 1,4,5-Trisphosphate Receptors; D007425:Intracellular Membranes / Q000378:metabolism*; D051379:Mice; D009447:Neuroblastoma / Q000378:metabolism* / Q000473:pathology; D015345:Oligonucleotide Probes / Q000235:genetics; D011794:Quercetin / Q000494:pharmacology; D051381:Rats; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism; D012769:Shock / Q000209:etiology / Q000378:metabolism*; D014407:Tumor Cells, Cultured
chemical_list: D015220:Calcium Channels; D006360:Heat-Shock Proteins; D053496:Inositol 1,4,5-Trisphosphate Receptors; D015345:Oligonucleotide Probes; D018160:Receptors, Cytoplasmic and Nuclear; D015544:Inositol 1,4,5-Trisphosphate; D011794:Quercetin; D001920:Bradykinin; D002118:Calcium