ArticlePancreas
Activation of the Nuclear Factor-kappa B Signaling Pathway Damages the Epithelial Barrier in the Human Pancreatic Ductal Adenocarcinoma Cell Line HPAF-II.
Article in Pancreas. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed, 7 citations in OpenAlex.
- Inhibition of MLCK‑mediated migration and invasion in human endometriosis stromal cells by NF‑κB inhibitor DHMEQ.Molecular medicine reports · 2023Article
- HO-1/CO Maintains Intestinal Barrier Integrity through NF-Oxidative medicine and cellular longevity · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesInjury of the pancreatic duct epithelial barrier plays a critical role in the development of acute pancreatitis. The activity of the nuclear factor-kappa B (NF-κB) pathway is involved in the disruption of the pancreatic duct epithelial barrier. This study investigated how NF-κB impacts the dysfunction of the pancreatic duct epithelial barrier.
methodsA human pancreatic ductal adenocarcinoma cell line was treated with tumor necrosis factor-alpha (TNF-α) and pyrrolidine dithiocarbamate. The expression levels of p65 and p-p65 were detected to evaluate NF-κB activity. Tricellulin (TRIC) expression levels were measured to assess the change in tight junction (TJ)-related proteins. The expression and localization of myosin light chain kinase (MLCK) were investigated. The structure of TJs and monolayer permeability were also examined.
resultsNF-κB was activated by TNF-α and suppressed by pyrrolidine dithiocarbamate. Activation of NF-κB upregulated the expression levels of TRIC and MLCK. Broadened TJs were observed after NF-κB was activated. Lower monolayer permeability was observed when NF-κB was suppressed.
conclusionsActivation of the NF-κB pathway induced by TNF-α leads to increased TRIC and MLCK expression, resulting in broadened TJs and high permeability, which contribute to damage to the pancreatic duct epithelial barrier.
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Registered trials
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