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Effect of Heat Shock on Intracellular Calcium Mobilization in Neuroblastoma × Glioma Hybrid Cells
Author(s) -
Katayama Shigenori,
Shuntoh Hisato,
Matsuyama Shogo,
Tanaka Chikako
Publication year - 1994
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1994.62062292.x
Subject(s) - thapsigargin , bradykinin receptor , calcium in biology , bradykinin , heat shock protein , intracellular , heat shock , microbiology and biotechnology , glioma , chemistry , receptor , biology , biochemistry , cancer research , gene
The effect of heat shock on agonist‐stimulated intracellular Ca 2+ mobilization and the expression of heat shock protein 72 (hsp72) in neuroblastoma × glioma hybrid cells (NG 108–15 cells) were examined. Hsp72 was expressed at 6 h after heat shock (42.5°C, 2 h), reached a maximum at 12 h, and decreased thereafter. Bradykinin‐induced [Ca 2+ ], 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 [Ca 2+ ] i rise was abolished and the [Ca 2+ ] 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 (IP 3 ) production was not altered by heat shock at 12 h after heat shock, whereas IP 3 receptor binding activity was reduced to 45.3%. In the presence of quercetin or antisense oligodeoxyribonucleotide, IP 3 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 IPs‐mediated intracellular Ca 2+ signal transduction system and that hsp72 is involved in the recovery of bradykinin‐induced [Ca 2+ ] i rise.