ArticleJournal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract2006
In vitro evidence for role of ERK, p38, and JNK in exocrine pancreatic cytokine production.
Article in Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 37 citations in OpenAlex.
- Review
- The Peptide-Drug Conjugate M1pep-Tasquinimod Ameliorates Acute Pancreatitis via Selectively Clearing M1-like Macrophages.Biomaterials research · 2025Article
- Article
- Molecular Mechanism of Pancreatic Stellate Cells Activation in Chronic Pancreatitis and Pancreatic Cancer.Journal of Cancer · 2020Review
- Curcumin protects the pancreas from acute pancreatitis via the mitogen‑activated protein kinase signaling pathway.Molecular medicine reports · 2019Article
- Protective Effects of Calcitonin Gene-Related Peptide-Mediated p38 Mitogen-Activated Protein Kinase Pathway on Severe Acute Pancreatitis in Rats.Digestive diseases and sciences · 2019Article
- Cyclic AMP-dependent protein kinase A and EPAC mediate VIP and secretin stimulation of PAK4 and activation of NaAmerican journal of physiology. Gastrointestinal and liver physiology · 2019Article
- Phytoceuticals in Acute Pancreatitis: Targeting the Balance between Apoptosis and Necrosis.Evidence-based complementary and alternative medicine : eCAM · 2018Review
- Reduced Pancreatic Exocrine Function and Organellar Disarray in a Canine Model of Acute Pancreatitis.PloS one · 2016Article
- Evidence for a role of mitogen-activated protein kinases in the treatment of experimental acute pancreatitis.World journal of gastroenterology · 2014Review
- Src Dependent Pancreatic Acinar Injury Can Be Initiated Independent of an Increase in Cytosolic Calcium.PloS one · 2013Article
- Systemic inflammation with multiorgan dysfunction is the cause of death in murine ligation-induced acute pancreatitis.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2011Article
- Potential role of NADPH oxidase-mediated activation of Jak2/Stat3 and mitogen-activated protein kinases and expression of TGF-β1 in the pathophysiology of acute pancreatitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2011Article
- Nuclear factor kappa B-dependent gene transcription in cholecystokinin- and tumor necrosis factor-alpha-stimulated isolated acinar cells is regulated by p38 mitogen-activated protein kinase.American journal of surgery · 2010Article
- Murine pancreatic duct ligation induces stress kinase activation, acute pancreatitis, and acute lung injury.American journal of surgery · 2008Article
- Bile and pancreatic juice exclusion activates acinar stress kinases and exacerbates gallstone pancreatitis.Surgery · 2008Review
- Enteral exclusion increases MAP kinase activation and cytokine production in a model of gallstone pancreatitis.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2008Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elucidation of mechanisms of acinar cell cytokine production is essential for a better understanding of acute pancreatitis pathogenesis. We hypothesize that the stress kinases ERK, p38, and JNK play an important role in acinar cell cytokine production. Rat pancreatic fragments were incubated with 100 nM concentration of the cholecystokinin analog caerulein or 100 nM caerulein and specific ERK inhibitor (100 microM PD98059), specific p38 inhibitor (10 microM SB203580), or specific JNK inhibitor (20 microM SP600125). After 3 hours of caerulein treatment, pancreatic fragments were homogenized and assayed for total and phosphorylated ERK, p38, and JNK, and for tumor necrosis factor-alpha or interleukin-1beta concentrations (ELISA). Pancreatic fragments stimulated with caerulein showed activation of ERK, p38, and JNK and increased cytokine concentrations (ANOVA, P<0.05). Specific stress kinase inhibitors significantly attenuated caerulein-induced activation of the corresponding stress kinase and cytokine production; however, the effect of the JNK inhibitor was comparatively less convincing. Increased activation of ERK, p38, and JNK in pancreatic fragments was not associated with significant increases in total ERK, total p38, or total JNK concentrations. The stress kinases ERK and p38 play an important role in caerulein-stimulated exocrine pancreatic overproduction of cytokines. The role of JNK needs further evaluation in this experimental model.
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