ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2012
c-Jun/AP-1 is required for CCK-induced pancreatic acinar cell dedifferentiation and DNA synthesis in vitro.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2012. 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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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
12 citing papers in PubMed, 20 citations in OpenAlex.
- Review
- Spatio-temporal expression pattern and role of the tight junction protein MarvelD3 in pancreas development and function.Scientific reports · 2021Article
- Necroptosis protects against exacerbation of acute pancreatitis.Cell death & disease · 2021Article
- Expression and Functional Characterization ofGenes · 2021Article
- Group II p21-activated kinase, PAK4, is needed for activation of focal adhesion kinases, MAPK, GSK3, and β-catenin in rat pancreatic acinar cells.American journal of physiology. Gastrointestinal and liver physiology · 2020Article
- Genetics, Cell Biology, and Pathophysiology of Pancreatitis.Gastroenterology · 2019Review
- Src kinases play a novel dual role in acute pancreatitis affecting severity but no role in stimulated enzyme secretion.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Reserve stem cells: Differentiated cells reprogram to fuel repair, metaplasia, and neoplasia in the adult gastrointestinal tract.Science signaling · 2015Review
- Can Bayliss and Starling gut hormones cure a worldwide pandemic?The Journal of physiology · 2014Article
- ERK activation is required for CCK-mediated pancreatic adaptive growth in mice.American journal of physiology. Gastrointestinal and liver physiology · 2014Article
- MAPK signaling is required for dedifferentiation of acinar cells and development of pancreatic intraepithelial neoplasia in mice.Gastroenterology · 2014Article
- Cholecystokinin and pancreatic cancer: the chicken or the egg?American journal of physiology. Gastrointestinal and liver physiology · 2014Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Endogenous CCK plays an important role in pancreatic regeneration after pancreatitis. We used primary culture of mouse pancreatic acinar cells to evaluate the effect of CCK on acinar cell morphology and gene expression and to determine signaling pathways required for proliferation of acinar cells in vitro. Over 4 days in culture, cells grew out from acini and formed patches of monolayer, which displayed a reduced expression of acinar cell markers including digestive enzymes and Mist1 and an increased expression of ductal and embryonic markers, including cytokeratin 7, β-catenin, E-cadherin, pdx-1, and nestin. There was no appearance of stellate cell markers. CCK enhanced cellular spreading, DNA synthesis, and cyclin D1 expression. When signaling pathways were evaluated, CCK stimulation increased c-Jun expression, JNK and ERK activity, and AP-1 activation. Chemical inhibitors of JNK and ERK pathways, dominant-negative JNK and c-Jun, and c-Jun shRNA significantly inhibited CCK-induced DNA synthesis, CCK-induced AP-1 activation, and cyclin D1 expression. Furthermore, dominant-negative c-Jun reduced the increased expression of β-catenin and the decreased expression of amylase during culture. These results show that MAPK/c-Jun/AP-1 pathway plays an important role in pancreatic acinar cell dedifferentiation and proliferation in culture. Monolayer culture can serve as a model to study acinar cell proliferation similar to regeneration after pancreatitis in vivo.
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Registered trials
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