Calcium signalling and pancreatic cell death: apoptosis or necrosis?

Criddle, David N.; Gerasimenko, Julia Vladimirovna; Baumgartner, Heidi K.; Jaffar, Mohammed; Voronina, Svetlana; Sutton, Robert; Petersen, O. H.; Gerasimenko, Oleg Vsevolodovich

doi:10.1038/sj.cdd.4402150

Cited by 161 publications

(155 citation statements)

References 86 publications

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“…Genetic or pharmacologic blockade of PARP inhibits necrosis and demonstrates a reduced pancreatitis response (43). In addition to the passive ATP depletion-mediated mechanisms, several active mechanisms (for example, oxidative stress, calcium overload, mitochondrial permeability transition pore opening and cathepsin release) also participate in the regulation of the necrotic process in AP (34,44,45). The actual mechanisms of necrosis involved in the development of sequential cellular and organ response in AP need further investigation.…”

Section: Necrosismentioning

confidence: 99%

Cell Death and DAMPs in Acute Pancreatitis

Kang

Lotze

Zeh

et al. 2014

Mol Med

124

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The pancreas is a dual-purpose gland with exocrine and endocrine functions. The exocrine pancreas produces digestive proteases in inactive proenzyme form, namely zymogens. The pancreas is normally able to protect itself from zymogen activation by synthesis of protease inhibitors such as pancreatic secretory trypsin inhibitor and serine protease inhibitor (for example, SPINK1/Spink3). By contrast, pancreatic autodigestion and subsequent AP is initiated once these defenses are impaired. In studies of rodent models (for example, repetitive cerulein or L-arginine injections, choline-deficient ethionine supplementation [CDE] diet, perfusion of taurocholate into the biliary or pancreatic duct and surgical ligation or infusion of pancreatic duct models), some essential pathogenic AP events have been identified (see Figure 1) (15,16).The development of AP involves a complex cascade of events (17), which start with injury or disruption of the pan- Cell Death and DAMPs in Acute PancreatitisRui Kang, Michael T Lotze, Herbert J Zeh, Timothy R Billiar, and Daolin Tang Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America Cell death and inflammation are key pathologic responses of acute pancreatitis (AP), the leading cause of hospital admissions for gastrointestinal disorders. It is becoming increasingly clear that damage-associated molecular pattern molecules (DAMPs) play an important role in the pathogenesis of AP by linking local tissue damage to systemic inflammation syndrome. Endogenous DAMPs released from dead, dying or injured cells initiate and extend sterile inflammation via specific pattern recognition receptors. Inhibition of the release and activity of DAMPs (for example, high mobility group box 1, DNA, histones and adenosine triphosphate) provides significant protection against experimental AP . Moreover, increased serum levels of DAMPs in patients with AP correlate with disease severity. These findings provide novel insight into the mechanism, diagnosis and management of AP . DAMPs might be an attractive therapeutic target in AP.

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Section: Necrosismentioning

confidence: 99%

Cell Death and DAMPs in Acute Pancreatitis

Kang

Lotze

Zeh

et al. 2014

Mol Med

124

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“…If death of pancreatic acinar cells occurs in the mode of apoptosis, the cell membrane is intact and there is no release of inflammatory mediators and pancreatin, the inflammatory reaction may be mild [4] . However, if death of pancreatic acinar cells occurs in the mode of oncosis, various pancreatin and inflammatory mediators may release, thus causing a variety of inflammatory cell aggregations and inducing intense inflammatory reactions [5] . If we can induce apoptosis and reduce oncosis, intense inflammatory reactions may be inhibited.…”

Section: Introductionmentioning

confidence: 99%

Induction of apoptosis by artemisinin relieving the severity of inflammation in caerulein-induced acute pancreatitis

Zhao

Xue²,

Zheng³

et al. 2007

WJG

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AIM:To observe the apoptosis and oncosis of pancreatic acinar cells and secondary inflammatory reaction in pancreatic tissue from rats with acute pancreatitis (AP), and the influences of artemisinin on them. METHODS: AP was induced by 4 intraperitonealinjections of caerulein at 1 h intervals. To induce apoptosis, solution of artemisinin (50 mg/kg) was given intraperitoneally 1, 12, 24 and 36 h after the last caerulein injection. Histological examination of impairment of pancreatic tissue and detection of serum amylase were performed to evaluate the severity of acute pancreatitis. Apoptosis and oncosis were detected with acridine orange (AO) and ethylene dibromide (EB) staining. Caspase-3 and myeloperoxidase (MPO) activity were measured by colorimetric assay. Nuclear factor-kappa B (NF-κB) activation was detected by flow cytometry. Macrophage inflammatory protein-1α (MIP-1α) protein was measured by Western blot. Interleukin-1β (IL-1β) mRNA was detected by RT-PCR. RESULTS:Addition of artemisinin increased the number of apoptotic cells (11.7% ± 1.4% vs 6.3% ± 0.7%, P < 0.05), while reduced the number of oncotic cells (13.0% ± 2.4% vs 17.5% ± 2.2%, P < 0.05). The activity of caspase-3 speeded up (1.52 ± 0.21 vs 1.03 ± 0.08, P < 0.05), the pancreas pathological impairment was relieved (3.0 ± 0.5 vs 4.0 ± 0.5, P < 0.05) and the level of serum amylase decreased (5642 ± 721 U/dL vs 7821 ± 653 U/dL, P < 0.05). The activation of NF-κB (29% ± 4.1% vs 42% ± 5.8%), MIP-1α protein (3.7 ± 0.5 vs 5.8 ± 0.7), MPO (0.52 ± 0.06 U/g vs 0.68 ± 0.09 U/g), IL-1β mRNA (1.7 ± 0.3 vs 2.4 ± 0.4) in the apoptosis inducing group was obviously decreased (P < 0.05).

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“…These guiding concepts have inspired the articles presented in this issue of Cell Death & Differentiation. [24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39] This collection of reviews, dealing with mechanisms of cells and tissue damage and repair, is based on the invited lectures given at an international conference on this broad topic. This conference, which was organized jointly by Academia Europaea and The Klaus Tschira Foundation, took place in Heidelberg, Germany in March 2007 (Figure 1).…”

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confidence: 99%