Involvement of calmodulin in the activation of store-operated Ca2+ entry in rat hepatocytes.
The possible participation of calmodulin in the activation of store-operated Ca2+ entry (SOC) in single rat hepatocytes was investigated microspectrofluorimetrically. SOC was triggered after discharging intracellular Ca2+ stores using the endoplasmic reticulum Ca2+-ATPase inhibitor thapsigargin in the absence of external Ca2+. Re-admission of bath Ca2+ caused a rapid and pronounced Ca2+ entry. The calmodulin antagonists calmidazolium or CGS 9343B applied before the thapsigargin treatment inhibited SOC, whereas they were ineffective when added after the thapsigargin-induced Ca2+ transient. This study suggests that activation of calmodulin after the elevation of cytosolic Ca2+ associated with the emptying of Ca2+ stores is involved in the triggering of SOC in hepatocytes.
Cao
Y
Y
Institute of Pharmacology, University of Berne, Switzerland.
Chatton
J Y
JY
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D000252:Calcium-Transporting ATPases / Q000037:antagonists & inhibitors*; D002147:Calmodulin / Q000037:antagonists & inhibitors / Q000378:metabolism*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D007093:Imidazoles / Q000494:pharmacology; D008099:Liver / Q000166:cytology / Q000378:metabolism*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction; D019284:Thapsigargin / Q000494:pharmacology
D002147:Calmodulin; D004791:Enzyme Inhibitors; D007093:Imidazoles; C031938:calmidazolium; D019284:Thapsigargin; D000252:Calcium-Transporting ATPases; D002118:Calcium