Bile acids induce calcium signals in mouse pancreatic acinar cells: implications for bile-induced pancreatic pathology.
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Review of experimental animal models of biliary acute pancreatitis and recent advances in basic researchNitric oxide signals are interlinked with calcium signals in normal pancreatic stellate cells upon oxidative stress and inflammationAberrant localization of intracellular organelles, Ca2+ signaling, and exocytosis in Mist1 null miceInhibitors of ORAI1 Prevent Cytosolic Calcium-Associated Injury of Human Pancreatic Acinar Cells and Acute Pancreatitis in 3 Mouse ModelsBile acids induce Ca2+ release from both the endoplasmic reticulum and acidic intracellular calcium stores through activation of inositol trisphosphate receptors and ryanodine receptors.The ryanodine receptor is expressed in human pancreatic acinar cells and contributes to acinar cell injuryCalcium signaling of pancreatic acinar cells in the pathogenesis of pancreatitis.The role of Ca2+ influx in endocytic vacuole formation in pancreatic acinar cellsAcinar Cell Production of Leukotriene B4 Contributes to Development of Neurogenic Pancreatitis in MiceBone Marrow-Derived Mesenchymal Stem Cells Repair Necrotic Pancreatic Tissue and Promote Angiogenesis by Secreting Cellular Growth Factors Involved in the SDF-1 α /CXCR4 Axis in RatsCalcium and reactive oxygen species in acute pancreatitis: friend or foe?Value of genetic testing in the management of pancreatitisTwenty years of calcium imaging: cell physiology to dye for.Bile Acids Trigger GLP-1 Release Predominantly by Accessing Basolaterally Located G Protein-Coupled Bile Acid Receptors.A mouse model of acute biliary pancreatitis induced by retrograde pancreatic duct infusion of Na-taurocholate.Interaction of gut microbiota with bile acid metabolism and its influence on disease states.Mechanisms of acinar cell injury in acute pancreatitis.Mechanisms of disease: Advances in understanding the mechanisms leading to chronic pancreatitis.Bile acid interactions with cholangiocytes.Bile acids induce pancreatic acinar cell injury and pancreatitis by activating calcineurin.Ethanol toxicity in pancreatic acinar cells: mediation by nonoxidative fatty acid metabolitesCalcium and adenosine triphosphate control of cellular pathology: asparaginase-induced pancreatitis elicited via protease-activated receptor 2Ryanodine receptors contribute to bile acid-induced pathological calcium signaling and pancreatitis in mice.Pancreatic acinar cell nuclear factor κB activation because of bile acid exposure is dependent on calcineurin.Cluster of differentiation 38 (CD38) mediates bile acid-induced acinar cell injury and pancreatitis through cyclic ADP-ribose and intracellular calcium releaseEffect of Chaiqinchengqi decoction on sarco/endoplasmic reticulum Ca2+-ATPase mRNA expression of pancreatic tissues in acute pancreatitis ratsNecroptosis Is an Important Severity Determinant and Potential Therapeutic Target in Experimental Severe Pancreatitis.One compound of saponins from Disocorea zingiberensis protected against experimental acute pancreatitis by preventing mitochondria-mediated necrosis.Ca2+ signaling in pancreatic acinar cells: physiology and pathophysiology.Caffeine protects against experimental acute pancreatitis by inhibition of inositol 1,4,5-trisphosphate receptor-mediated Ca2+ release.Central role of mitochondrial injury in the pathogenesis of acute pancreatitis.Role of ion transporters in the bile acid-induced esophageal injury.Lycopene protects pancreatic acinar cells against severe acute pancreatitis by abating the oxidative stress through JNK pathway.Bile acids enhance invasiveness of Cryptosporidium spp. into cultured cells.Bile acids induce necrosis in pancreatic stellate cells dependent on calcium entry and sodium-driven bile uptake.Biliary acute pancreatitis in mice is mediated by the G-protein-coupled cell surface bile acid receptor Gpbar1.Ca(2+) signals mediated by bradykinin type 2 receptors in normal pancreatic stellate cells can be inhibited by specific Ca(2+) channel blockade.Dynamic changes in cytosolic and mitochondrial ATP levels in pancreatic acinar cells.Effects of secretagogues and bile acids on mitochondrial membrane potential of pancreatic acinar cells: comparison of different modes of evaluating DeltaPsim.A novel, protective role of ursodeoxycholate in bile-induced pancreatic ductal injury.
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P2860
Bile acids induce calcium signals in mouse pancreatic acinar cells: implications for bile-induced pancreatic pathology.
description
2002 nî lūn-bûn
@nan
2002年の論文
@ja
2002年学术文章
@wuu
2002年学术文章
@zh-cn
2002年学术文章
@zh-hans
2002年学术文章
@zh-my
2002年学术文章
@zh-sg
2002年學術文章
@yue
2002年學術文章
@zh
2002年學術文章
@zh-hant
name
Bile acids induce calcium sign ...... -induced pancreatic pathology.
@en
Bile acids induce calcium sign ...... -induced pancreatic pathology.
@nl
type
label
Bile acids induce calcium sign ...... -induced pancreatic pathology.
@en
Bile acids induce calcium sign ...... -induced pancreatic pathology.
@nl
prefLabel
Bile acids induce calcium sign ...... -induced pancreatic pathology.
@en
Bile acids induce calcium sign ...... -induced pancreatic pathology.
@nl
P2093
P2860
P1476
Bile acids induce calcium sign ...... e-induced pancreatic pathology
@en
P2093
Ole H Petersen
Rebecca Longbottom
Robert Sutton
Svetlana Voronina
P2860
P356
10.1113/JPHYSIOL.2002.017525
P407
P577
2002-04-01T00:00:00Z