scholarly journals Angiotensin-(1–7) attenuates caerulein-induced pancreatic acinar cell apoptosis

2017 ◽  
Vol 16 (3) ◽  
pp. 3455-3460 ◽  
Author(s):  
Lijian Cui ◽  
Ruixia Liu ◽  
Chunyun Li ◽  
Xiaozheng Yu ◽  
Xiaoya Liu ◽  
...  
Keyword(s):  
Acinar Cell ◽  
Cell Apoptosis ◽  
Pancreatic Acinar Cell

Crambene induces pancreatic acinar cell apoptosis via the activation of mitochondrial pathway

2006 ◽  
Vol 291 (1) ◽  
pp. G95-G101 ◽  
Author(s):  
Yang Cao ◽  
Sharmila Adhikari ◽  
Abel Damien Ang ◽  
Marie Véronique Clément ◽  
Matthew Wallig ◽  
...  
Keyword(s):  
Acinar Cell ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Fas Ligand ◽  
Annexin V ◽  
Acinar Cells ◽  
Mitochondrial Pathway ◽  
Pancreatic Acinar Cell ◽  
Pancreatic Acinar Cells ◽  
Pancreatic Acini

We investigated the apoptotic pathway activated by crambene (1-cyano-2-hydroxy-3-butene), a plant nitrile, on pancreatic acinar cells. As evidenced by annexin V-FITC staining, crambene treatment for 3 h induced the apoptosis but not necrosis of pancreatic acini. Caspase-3, -8, and -9 activities in acini treated with crambene were significantly higher than in untreated acini. Treatment with caspase-3, -8, and -9 inhibitors inhibited annexin V staining, as well as caspase-3 activity, pointing to an important role of these caspases in crambene-induced acinar cell apoptosis. The mitochondrial membrane potential was collapsed, and cytochrome c was released from the mitochondria in crambene-treated acini. Neither TNF-α nor Fas ligand levels were changed in pancreatic acinar cells after crambene treatment. These results provide evidence for the induction of pancreatic acinar cell apoptosis in vitro by crambene and suggest the involvement of mitochondrial pathway in pancreatic acinar cell apoptosis.

Mechanism of induction of pancreatic acinar cell apoptosis by hydrogen sulfide

2006 ◽  
Vol 291 (3) ◽  
pp. C503-C510 ◽  
Author(s):  
Yang Cao ◽  
Sharmila Adhikari ◽  
Abel Damien Ang ◽  
Philip K. Moore ◽  
Madhav Bhatia
Keyword(s):  
Acinar Cell ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Death Receptor ◽  
Annexin V ◽  
Pancreatic Acinar Cell ◽  
Apoptotic Pathway ◽  
Pancreatic Acini ◽  
Phosphatidylserine Externalization

The present study investigated the mechanism of mouse pancreatic acinar cell apoptosis induced by H2S in an in vitro system, using isolated pancreatic acini. Treatment of pancreatic acini with 10 μM NaHS (a donor of H2S) for 3 h caused phosphatidylserine externalization as shown by annexin V binding, an indicator of early stages of apoptosis. This treatment also resulted in the activation of the caspase cascade and major changes at the mitochondrial level. Caspase-3, -8, and -9 activities were stimulated by H2S treatment. Treatment with inhibitors of caspase-3, -8, and -9 significantly inhibited H2S-induced phosphatidylserine externalization as shown by reduced annexin V staining. The mitochondrial membrane potential was collapsed in H2S-treated acini as evidenced by fluorescence microscopy and quantitative analysis. Furthermore, the treatment of acini with H2S caused the release of cytochrome c by the mitochondria. To investigate the mechanism underlying pancreatic acinar cell apoptosis, we also characterized the protein expression of a range of molecules that are each known to influence the apoptotic pathway. Among proapoptotic proteins, Bax expression was activated in H2S-treated cells but not Bid, and the antiapoptotic proteins Bcl-XL and Bcl-2 did not show any activation in pancreatic acinar cell apoptosis. The death effector domain-containing protein Flip is downregulated in H2S-treated acini. These results demonstrate the induction of pancreatic acinar cell apoptosis in vitro by H2S and the involvement of both mitochondrial and death receptor pathways in the process of apoptosis.

scholarly journals ATF6 regulates the development of chronic pancreatitis by inducing p53-mediated apoptosis

2019 ◽  
Vol 10 (9) ◽  
Author(s):  
Lei Zhou ◽  
Jie-hui Tan ◽  
Rong-chang Cao ◽  
Jia Xu ◽  
Xue-mei Chen ◽  
...  
Keyword(s):  
Chronic Pancreatitis ◽  
Er Stress ◽  
Acinar Cell ◽  
Cell Apoptosis ◽  
Pancreatic Acinar Cell ◽  
Inflammatory Factors ◽  
Marker Genes ◽  
Inflammatory Disorder ◽  
P53 Expression ◽  
Tnf Α

Abstract Chronic pancreatitis (CP) is a progressive, recurrent inflammatory disorder of the pancreas. Initiation and progression of CP can result from serine protease 1 (PRSS1) overaccumulation and the ensuing endoplasmic reticulum (ER) stress. However, how ER stress pathways regulate the development and progression of CP remains poorly understood. In the present study we aimed to elucidate the ER stress pathway involved in CP. We found high expression of the ER stress marker genes ATF6, XBP1, and CHOP in human clinical specimens. A humanized PRSS1 transgenic mouse was established and treated with caerulein to mimic the development of CP, as evidenced by pathogenic alterations, collagen deposition, and increased expression of the inflammatory factors IL-6, IL-1β, and TNF-α. ATF6, XBP1, and CHOP expression levels were also increased during CP development in this model. Acinar cell apoptosis was also significantly increased, accompanied by upregulated p53 expression. Inhibition of ATF6 or p53 suppressed the expression of inflammatory factors and progression of CP in the mouse model. Finally, we showed that p53 expression could be regulated by the ATF6/XBP1/CHOP axis to promote the development of CP. We therefore conclude that ATF6 signalling regulates CP progression by modulating pancreatic acinar cell apoptosis, which provides a target for ER stress-based diagnosis and treatment of CP.

Fas and fas ligand system as a mediator of pancreatic acinar cell apoptosis after pancreatic duct ligation

1998 ◽  
Vol 114 ◽  
pp. A511
Author(s):  
H. Yasuda ◽  
K. Kataoka ◽  
M. Moriguchi ◽  
K. Kashima ◽  
H. Ichimura ◽  
...  
Keyword(s):  
Pancreatic Duct ◽  
Acinar Cell ◽  
Cell Apoptosis ◽  
Fas Ligand ◽  
Pancreatic Acinar Cell ◽  
Ligand System ◽  
Pancreatic Duct Ligation ◽  
Duct Ligation
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