Faculty Opinions recommendation of Cluster of differentiation 38 (CD38) mediates bile acid-induced acinar cell injury and pancreatitis through cyclic ADP-ribose and intracellular calcium release.

2013 ◽  
Author(s):  
Julia Gerasimenko ◽  
Martyn Richard Charlesworth
Keyword(s):  
Bile Acid ◽  
Intracellular Calcium ◽  
Acinar Cell ◽  
Calcium Release ◽  
Cell Injury ◽  
Cyclic Adp Ribose ◽  
Intracellular Calcium Release ◽  
Cluster Of Differentiation

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.

Cyclic ADP-ribose production by CD38 regulates intracellular calcium release, extracellular calcium influx and chemotaxis in neutrophils and is required for bacterial clearance in vivo

2001 ◽  
Vol 7 (11) ◽  
pp. 1209-1216 ◽  
Author(s):  
Santiago Partida-Sánchez ◽  
Debra A. Cockayne ◽  
Simon Monard ◽  
Elaine L. Jacobson ◽  
Norman Oppenheimer ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Calcium Release ◽  
Calcium Influx ◽  
Extracellular Calcium ◽  
Bacterial Clearance ◽  
Cyclic Adp Ribose ◽  
Intracellular Calcium Release

scholarly journals Orientia tsutsugamushi Inhibits Apoptosis of Macrophages by Retarding Intracellular Calcium Release

2002 ◽  
Vol 70 (8) ◽  
pp. 4692-4696 ◽  
Author(s):  
Mee-Kyung Kim ◽  
Seung-Yong Seong ◽  
Ju-Young Seoh ◽  
Tae-Hee Han ◽  
Hyeon-Je Song ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Calcium Release ◽  
Cytosolic Calcium ◽  
Orientia Tsutsugamushi ◽  
Cytosolic Calcium Concentration ◽  
Infected Cells ◽  
Intracellular Calcium Release ◽  
Calcium Redistribution ◽  
In Cells

ABSTRACT Orientia tsutsugamushi shows both pro- and antiapoptotic activities in infected vertebrate cells. Apoptosis of THP-1 cells induced by beauvericin was inhibited by O. tsutsugamushi infection. Beauvericin-induced calcium redistribution was significantly reduced and retarded in cells infected with O. tsutsugamushi. Antiapoptotic activities of O. tsutsugamushi in infected cells are most probably due to inhibition of the increase in the cytosolic calcium concentration.

scholarly journals A Membrane Estrogen Receptor Mediates Intracellular Calcium Release in Astrocytes

Endocrinology ◽  
2004 ◽  
Vol 145 (8) ◽  
pp. 3788-3795 ◽  
Author(s):  
Victor V. Chaban ◽  
Alexander J. Lakhter ◽  
Paul Micevych
Keyword(s):  
Estrogen Receptor ◽  
Intracellular Calcium ◽  
Calcium Release ◽  
Intracellular Calcium Release

scholarly journals N-terminus oligomerization is conserved in intracellular calcium release channels

2014 ◽  
Vol 459 (2) ◽  
pp. 265-273 ◽  
Author(s):  
Spyros Zissimopoulos ◽  
Jason Marsh ◽  
Laurence Stannard ◽  
Monika Seidel ◽  
F. Anthony Lai
Keyword(s):  
Structure Function ◽  
Intracellular Calcium ◽  
Calcium Release ◽  
Function Parameter ◽  
Calcium Release Channels ◽  
Cellular Processes ◽  
N Terminus ◽  
Intracellular Calcium Release ◽  
Ca2 Channels

Intracellular Ca2+ channels are of paramount importance for numerous cellular processes. In the present paper we report on a novel N-terminus intersubunit interaction, an essential structure–function parameter, which is conserved in both families of intracellular Ca2+ channels.

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