A role for a pertussis toxin‐sensitive trimeric G‐protein in store‐operated Ca2+inflow in hepatocytes

Publisher Website
Google Scholar
Abstract
The mechanism of store‐operated Ca2+inflow in hepatocytes was investigated using fluo‐3 and fura‐2 to monitor changes in the concentration of intracellular free Ca2+in single cells, and 1‐(α‐glycerophosphoryl)‐myo‐inositol 4,5‐diphosphate, P4(5)‐1‐(2‐nitrophenyl)ethyl ester (‘caged’ GPIP2) and ‘caged’ guanosine 5′‐[γthio]triphosphate (GTPγS) (introduced into the cytoplasmic space by microinjection), thapsigargin and 2,5‐di‐tert‐butylhydroquinone (DBHQ) to stimulate Ca2+inflow. Photolysis of ‘caged’ GPIP2or ‘caged’ GTPγS stimulated Ca2+inflow. The abilities of GPIP2, thapsigargin and DBHQ to stimulate Ca2+inflow were inhibited by the pre‐treatment of hepatocytes with pertussis toxin in vivo for 36 h. Thapsigargin‐stimulated Ca2+inflow was also inhibited by guanosine 5′‐[β‐thio]diphosphate (GDPβS) (introduced by microinjection). It is concluded that, in hepatocytes, store‐operated Ca2+inflow induced by the actions of either inositol 1,4,5‐trisphosphate, thapsigargin or DBHQ requires a pertussis toxin‐sensitive trimeric G‐protein.