ArticleThe Journal of clinical investigation1997
Pancreatic acinar cells produce, release, and respond to tumor necrosis factor-alpha. Role in regulating cell death and pancreatitis.
Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers.
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Who cites it
130 citing papers in PubMed, 384 citations in OpenAlex.
- Article
- BCL2 inhibition in acute and chronic pancreatitis - is there a therapeutic perspective?Cell death discovery · 2026Review
- Aldosterone induced by chronic stress promotes pancreatic steatosis in young male rats.Cell and tissue research · 2026Article
- Visceral fat lipolysis by pancreatic lipases worsens heart failure.Cell reports. Medicine · 2025Article
- Potential causal association between gut microbiota, inflammatory cytokines, and acute pancreatitis: A Mendelian randomization study.Journal of intensive medicine · 2025Article
- Pentraxin3 exacerbates acute pancreatitis injury by inhibiting oxidative phosphorylation pathway.Scientific reports · 2025Article
- Alcohol promotes CPT1A-induced lipid metabolism disorder to sentinel-regulate acute pancreatitis.European journal of medical research · 2025Article
- Alterations in exocrine pancreatic function after acute pancreatitis.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2024Review
- Irisin Ameliorate Acute Pancreatitis and Acinar Cell Viability through Modulation of the Unfolded Protein Response (UPR) and PPARγ-PGC1α-FNDC5 Pathways.Biomolecules · 2024Article
- Pancreatic Ubap2 deletion regulates glucose tolerance, inflammation, and protection from cerulein-induced pancreatitis.Cancer letters · 2023Article
- Krüppel-like Factor 5 Plays an Important Role in the Pathogenesis of Chronic Pancreatitis.Cancers · 2023Article
- IRAK3-mediated suppression of pro-inflammatory MyD88/IRAK signaling affects disease severity in acute pancreatitis.Scientific reports · 2023Article
- Administration of Warfarin Inhibits the Development of Cerulein-Induced Edematous Acute Pancreatitis in Rats.Biomolecules · 2023Article
- Repetitive Cerulein-Induced Chronic Pancreatitis in Growing Pigs-A Pilot Study.International journal of molecular sciences · 2023Article
- Optogenetic stimulation of the brainstem dorsal motor nucleus ameliorates acute pancreatitis.Frontiers in immunology · 2023Article
- Heart Failure and Pancreas Exocrine Insufficiency: Pathophysiological Mechanisms and Clinical Point of View.Journal of clinical medicine · 2022Review
- Understanding Necroptosis in Pancreatic Diseases.Biomolecules · 2022Review
- Exposure to binge ethanol and fatty acid ethyl esters exacerbates chronic ethanol-induced pancreatic injury in hepatic alcohol dehydrogenase-deficient deer mice.American journal of physiology. Gastrointestinal and liver physiology · 2022Article
- Endoplasmic reticulum stress promoted acinar cell necroptosis in acute pancreatitis through cathepsinB-mediated AP-1 activation.Frontiers in immunology · 2022Article
- Roles, detection, and visualization of neutrophil extracellular traps in acute pancreatitis.Frontiers in immunology · 2022Review
70 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to determine whether tumor necrosis factor-alpha (TNFalpha) and receptors for TNFalpha are expressed in the exocrine pancreas, and whether pancreatic acinar cells release and respond to TNFalpha. Reverse transcription PCR, immunoprecipitation, and Western blot analysis demonstrated the presence of TNFalpha and 55- and 75-kD TNFalpha receptors in pancreas from control rats, rats with experimental pancreatitis induced by supramaximal doses of cerulein, and in isolated pancreatic acini. Immunohistochemistry showed TNFalpha presence in pancreatic acinar cells. ELISA and bioassay measurements of TNFalpha indicated its release from pancreatic acinar cells during incubation in primary culture. Acinar cells responded to TNFalpha. TNFalpha potentiated NF-kappaB translocation into the nucleus and stimulated apoptosis in isolated acini while not affecting LDH release. In vivo studies demonstrated that neutralization of TNFalpha with an antibody produced a mild improvement in the parameters of cerulein-induced pancreatitis. However, TNFalpha neutralization greatly inhibited apoptosis in a modification of the cerulein model of pancreatitis which is associated with a high percentage of apoptotic cell death. The results indicate that pancreatic acinar cells produce, release, and respond to TNFalpha. This cytokine regulates apoptosis in both isolated pancreatic acini and experimental pancreatitis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.