ArticleAmerican journal of surgery2010
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.
Article in American journal of surgery, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Review
- Apocynin Attenuates Acute Kidney Injury and Inflammation in Rats with Acute Hypertriglyceridemic Pancreatitis.Digestive diseases and sciences · 2020Article
- Involvement of the PI3K/Akt/NF-BioMed research international · 2017Article
- Severity of pancreatitis‑associated intestinal mucosal barrier injury is reduced following treatment with the NADPH oxidase inhibitor apocynin.Molecular medicine reports · 2016Article
- NADPH Oxidase Inhibitor Apocynin Attenuates PCB153-Induced Thyroid Injury in Rats.International journal of endocrinology · 2016Article
- Pancreatic Acinar Cells Employ miRNAs as Mediators of Intercellular Communication to Participate in the Regulation of Pancreatitis-Associated Macrophage Activation.Mediators of inflammation · 2016Article
- Effect of emodin on endoplasmic reticulum stress in rats with severe acute pancreatitis.Inflammation · 2013Article
- The novel cytokine interleukin-33 activates acinar cell proinflammatory pathways and induces acute pancreatic inflammation in mice.PloS one · 2013Article
- Pathogenic mechanisms of acute pancreatitis.Current opinion in gastroenterology · 2012Review
- p38 Mitogen-activated protein kinase modulates exocrine secretion in rabbit lacrimal gland.Cellular & molecular biology letters · 2012Article
- Molecular mechanisms of pancreatic injury.Current opinion in gastroenterology · 2011Review
- Dominant negative p38 mitogen-activated protein kinase expression inhibits NF-kappaB activation in AR42J cells.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2010Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundMitogen-activated protein (MAP) kinases and nuclear factor kappa B (NF-kappaB) are implicated in early stages of acute pancreatitis pathogenesis. We investigated the relationship between the p38 MAP kinase and NF-kappaB in isolated acinar cells.
methodsIsolated rodent acinar cells were stimulated with agonists after infection with an adenovector containing a luciferase promoter driven only by NF-kappaB and an adenovector containing the dominant negative (DN) form of p38 (empty vector in controls).
resultsInitial immunoblots confirmed that the agonist stimulated p38 activation in acinar cells was substantially attenuated by DN p38 overexpression. Stimulation of native cholecystokinin (CCK)-A receptors or tumor necrosis factor-alpha (TNF-alpha) receptors promoted a significant increase in NF-kappaB-dependent gene transcription in cells infected with the empty vector, while overexpression of DN p38 significantly abrogated NF-kappaB-dependent luciferase activity.
conclusionsThese findings support our hypothesis that p38 is involved in the activation of proinflammatory nuclear transcription factors such as NF-kappaB in pancreatic exocrine cells.
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