Cyclic ADP-ribose-dependent Ca2+ release is modulated by free [Ca2+] in the scallop sarcoplasmic reticulum.
Cyclic ADP-ribose (cADPR) elicits calcium-induced calcium release (CICR) in a variety of cell types. We studied the effect of cADPR on Ca2+ release in muscle cells by incubating SR vesicles from scallop (Pecten jacobaeus) adductor muscle in the presence of the Ca2+ tracer fluo-3. Exposure of SR to cADPR (20 microM) produced Ca2+ release, which was a function of free [Ca2+] in a range between about 150 and 1000 nM, indicating an involvement of ryanodine-sensitive Ca2+ channels. This Ca2+ release was not significantly enhanced by calmodulin (7 micrograms/ml), but it was enhanced by equimolar addition of noncyclic ADPR. Also, the Ca2+ release elicited by cADPR/ADPR was a function of free [Ca2+] in a range between about 150 and 3000 nM, over which Ca2+ was inhibitory. cADPR self-inactivation was observed at low free [Ca2+] (about 150 nM), but it tended to disappear upon [Ca2+] elevation (about 250 nM). Caffeine or ryanodine induced a Ca2+ release which was ruthenium red (2.5 microM) sensitive at low [Ca2+]. However, the Ca2+ release induced by either ryanodine or cADPR was no longer ruthenium red sensitive when free [Ca2+] was increased. Based on these data, a model is proposed for Ca2+ signaling in muscle cells, where a steady-state cADPR level would trigger Ca2+ release when free [Ca2+] does reach a threshold slightly above its resting level, hence producing cascade RyR recruitment along SR cisternae from initial Ca2+ signaling sites.
Panfoli
I
I
Istituto Policattedra di Chimica Biologica, Università di Genova, V. le Benedetto XV 1, Genova, 16132, Italy.
Burlando
B
B
Viarengo
A
A
D036541:ADP-ribosyl Cyclase; D051997:ADP-ribosyl Cyclase 1; D000246:Adenosine Diphosphate Ribose / Q000031:analogs & derivatives* / Q000378:metabolism / Q000494:pharmacology; D000814:Aniline Compounds; D000818:Animals; D015703:Antigens, CD; D000943:Antigens, Differentiation / Q000378:metabolism; D002110:Caffeine / Q000037:antagonists & inhibitors / Q000494:pharmacology; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology; D020013:Calcium Signaling / Q000187:drug effects; D002147:Calmodulin / Q000494:pharmacology; D036563:Cyclic ADP-Ribose; D008954:Models, Biological; D008974:Mollusca / Q000187:drug effects / Q000378:metabolism*; D009244:NAD+ Nucleosidase / Q000378:metabolism; D012430:Ruthenium Red / Q000037:antagonists & inhibitors / Q000494:pharmacology; D012433:Ryanodine / Q000037:antagonists & inhibitors / Q000494:pharmacology; D019837:Ryanodine Receptor Calcium Release Channel / Q000502:physiology; D012519:Sarcoplasmic Reticulum / Q000187:drug effects / Q000378:metabolism*; D019284:Thapsigargin / Q000494:pharmacology; D014966:Xanthenes
D000814:Aniline Compounds; D015703:Antigens, CD; D000943:Antigens, Differentiation; D002147:Calmodulin; D019837:Ryanodine Receptor Calcium Release Channel; D014966:Xanthenes; D012430:Ruthenium Red; D036563:Cyclic ADP-Ribose; D012433:Ryanodine; D000246:Adenosine Diphosphate Ribose; C059715:Fluo-3; D000001:Calcimycin; D002110:Caffeine; D019284:Thapsigargin; D036541:ADP-ribosyl Cyclase; D009244:NAD+ Nucleosidase; D051997:ADP-ribosyl Cyclase 1; D002118:Calcium