The cyclic ADP ribose antagonist 8-NH 2 -cADP-ribose blocks cholecystokinin-evoked cytosolic Ca 2+ spiking in pancreatic acinar cells

1998 ◽  
Vol 435 (5) ◽  
pp. 746-748 ◽  
Author(s):  
J. M. Cancela ◽  
O. H. Petersen
Keyword(s):  
Acinar Cells ◽  
Pancreatic Acinar Cells ◽  
Cyclic Adp Ribose

scholarly journals Cluster of Differentiation 38 (CD38) Mediates Bile Acid-induced Acinar Cell Injury and Pancreatitis through Cyclic ADP-ribose and Intracellular Calcium Release

2013 ◽  
Vol 288 (38) ◽  
pp. 27128-27137 ◽  
Author(s):  
Abrahim I. Orabi ◽  
Kamaldeen A. Muili ◽  
Tanveer A. Javed ◽  
Shunqian Jin ◽  
Thottala Jayaraman ◽  
...  
Keyword(s):  
Bile Acid ◽  
Ryanodine Receptor ◽  
Acinar Cell ◽  
Calcium Release ◽  
Cell Injury ◽  
Acinar Cells ◽  
Pancreatic Acinar Cells ◽  
Iodide Uptake ◽  
Cyclic Adp Ribose ◽  
Intracellular Ca

Aberrant Ca2+ signals within pancreatic acinar cells are an early and critical feature in acute pancreatitis, yet it is unclear how these signals are generated. An important mediator of the aberrant Ca2+ signals due to bile acid exposure is the intracellular Ca2+ channel ryanodine receptor. One putative activator of the ryanodine receptor is the nucleotide second messenger cyclic ADP-ribose (cADPR), which is generated by an ectoenzyme ADP-ribosyl cyclase, CD38. In this study, we examined the role of CD38 and cADPR in acinar cell Ca2+ signals and acinar injury due to bile acids using pharmacologic inhibitors of CD38 and cADPR as well as mice deficient in Cd38 (Cd38−/−). Cytosolic Ca2+ signals were imaged using live time-lapse confocal microscopy in freshly isolated mouse acinar cells during perifusion with the bile acid taurolithocholic acid 3-sulfate (TLCS; 500 μm). To focus on intracellular Ca2+ release and to specifically exclude Ca2+ influx, cells were perifused in Ca2+-free medium. Cell injury was assessed by lactate dehydrogenase leakage and propidium iodide uptake. Pretreatment with either nicotinamide (20 mm) or the cADPR antagonist 8-Br-cADPR (30 μm) abrogated TLCS-induced Ca2+ signals and cell injury. TLCS-induced Ca2+ release and cell injury were reduced by 30 and 95%, respectively, in Cd38-deficient acinar cells compared with wild-type cells (p < 0.05). Cd38-deficient mice were protected against a model of bile acid infusion pancreatitis. In summary, these data indicate that CD38-cADPR mediates bile acid-induced pancreatitis and acinar cell injury through aberrant intracellular Ca2+ signaling.

Visualization of CCK-evoked exocytic events in rat pancreatic acinar cells

2001 ◽  
Vol 120 (5) ◽  
pp. A24-A24
Author(s):  
H GAISANO ◽  
L TANG ◽  
L SHEU ◽  
W TRIMBLE
Keyword(s):  
Acinar Cells ◽  
Pancreatic Acinar Cells

Effects of oncogenic K-ras on pancreatic acinar cells In vitro

2001 ◽  
Vol 120 (5) ◽  
pp. A722-A722
Author(s):  
Y BI ◽  
C LOGSDON
Keyword(s):  
Acinar Cells ◽  
Pancreatic Acinar Cells
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