Rapid increases in inositol trisphosphate and intracellular Ca++ after heat shock.
Heat shock (45 degrees C) caused a rapid (less than 1 min) release of inositol trisphosphate from the membranes of HA-1 CHO fibroblasts. The rise in inositol trisphosphate concentration was followed by an increase in intracellular free Ca++. In addition to the heat induced rise in intracellular free Ca++, we observed an increase in 45Ca++ influx following nonlethal heat shock (45 degrees C/10 min). The heat-induced increase in 45Ca++ influx was linearly related to membrane accumulation of phosphatidic acid, phosphoinositide metabolite that may be involved in Ca++ gating. These results suggest that the membrane may be the proximal target of heat shock; stimulation of rapid breakdown of polyphosphoinositides and subsequent increases in intracellular free Ca++ may provide a mechanistic insight into the pleiotropic effects of heat. In addition, the large increases in Ca++ influx could initiate a Ca++ dependent mechanism of thermal cell killing.
D000818:Animals; D001692:Biological Transport; D002118:Calcium / Q000378:metabolism*; D002460:Cell Line; D002462:Cell Membrane / Q000378:metabolism; D006224:Cricetinae; D003412:Cricetulus; D004075:Diglycerides / Q000378:metabolism; D005260:Female; D005347:Fibroblasts / Q000378:metabolism; D006358:Hot Temperature; D015544:Inositol 1,4,5-Trisphosphate; D007295:Inositol Phosphates / Q000378:metabolism*; D010712:Phosphatidic Acids / Q000378:metabolism; D013403:Sugar Phosphates / Q000378:metabolism*
D004075:Diglycerides; D007295:Inositol Phosphates; D010712:Phosphatidic Acids; D013403:Sugar Phosphates; D015544:Inositol 1,4,5-Trisphosphate; D002118:Calcium