ArticleThe American journal of pathology2006
Expression of the Notch signaling pathway and effect on exocrine cell proliferation in adult rat pancreas.
Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 80 citations in OpenAlex.
- Translating the blueprint of cell fate: eIF5A-mediated translation regulates cellular identity in the pancreas.Molecular metabolism · 2026Article
- Characterization of a pancreatic cancer GWAS signal suggests PDX1 buffers stress in the exocrine pancreas.medRxiv : the preprint server for health sciences · 2026Article
- Microbiome and MicroRNA or Long Non-Coding RNA-Two Modern Approaches to Understanding Pancreatic Ductal Adenocarcinoma.Journal of clinical medicine · 2023Review
- Genetics of irritable bowel syndrome: shifting gear via biobank-scale studies.Nature reviews. Gastroenterology & hepatology · 2022Review
- Matrix Metalloproteinases and Their Inhibitors in Pulmonary Fibrosis: EMMPRIN/CD147 Comes into Play.International journal of molecular sciences · 2022Review
- Loss ofLife science alliance · 2021Article
- Aberrant development of pancreatic beta cells derived from human iPSCs with FOXA2 deficiency.Cell death & disease · 2021Article
- Notch1 activation enhances proliferation via activation of cdc2 and delays differentiation of myeloid progenitors.Leukemia research · 2018Article
- Notch signaling is significantly suppressed in basal cell carcinomas and activation induces basal cell carcinoma cell apoptosis.Molecular medicine reports · 2017Article
- Growth Arrest Specific 2 (GAS2) is a Critical Mediator of Germ Cell Cyst Breakdown and Folliculogenesis in Mice.Scientific reports · 2016Article
- Cell therapies for pancreatic beta-cell replenishment.Italian journal of pediatrics · 2016Review
- Notch Signaling in Pancreatic Development.International journal of molecular sciences · 2015Review
- Reprogramming of human pancreatic exocrine cells to β-like cells.Cell death and differentiation · 2015Article
- Hnf1b controls pancreas morphogenesis and the generation of Ngn3+ endocrine progenitors.Development (Cambridge, England) · 2015Article
- Hes1: a key role in stemness, metastasis and multidrug resistance.Cancer biology & therapy · 2015Review
- Article
- Transient cytokine treatment induces acinar cell reprogramming and regenerates functional beta cell mass in diabetic mice.Nature biotechnology · 2014Article
- Article
- Significance of Notch1-signaling pathway in human pancreatic development and carcinogenesis.Applied immunohistochemistry & molecular morphology : AIMM · 2013Article
- Notch signaling in pancreatic cancer: oncogene or tumor suppressor?Trends in molecular medicine · 2013Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
When pancreatic tissue is injured after duct obstruction, acinoductal metaplasia is observed. Similar metaplastic changes occur when exocrine pancreatic cells are isolated and cultured. We demonstrate that under these experimental conditions the exocrine acinar cells lose their differentiated characteristics: expression of the acinar transcription factors p48/Ptf1alpha and Mist1 is decreased or lost, whereas expression of the embryonic transcription factor Pdx1 is increased. The receptors Notch1 and Notch2, members of the DSL family of Notch ligands, and the target genes in the Notch-signaling pathway Hes1, Hey1, and Hey2 become strongly up-regulated. We noted also reduced expression of Sel1L, a Notch repressor that is normally highly expressed in exocrine pancreas. Stimulation of Notch by its ligand Jagged1 diminished the proliferation of cultured metaplastic exocrine cells. Chemical inhibition of Notch signaling resulted in increased proliferation and induction of the cell-cycle regulator p21Cip1. This effect seems to be Hes1-independent and mainly coincides with decreased Hey1 and Hey2 mRNA expression. In conclusion, we demonstrate that during acinoductal metaplasia the Notch-signaling pathway is activated concomitantly with changes in transcription factor expression of pancreatic acinar cells. In addition, we show that Notch signaling is implicated in the suppression of proliferation of these metaplastic exocrine cells. The latter may be important in protection from neoplastic transformation.
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Registered trials
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.