ArticleThe American journal of pathology2013
Differences in the degree of cerulein-induced chronic pancreatitis in C57BL/6 mouse substrains lead to new insights in identification of potential risk factors in the development of chronic pancreatitis.
Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 69 citations in OpenAlex.
- PVNJournal of neuroinflammation · 2026Article
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- A Novel Insight into Chronic Pancreatitis Pathogenesis: the USP1/ITGB5 Axis-Mediated Stellate Cell Activation.Inflammation · 2026Article
- Strain-specific differences in cerulein-induced acute and recurrent acute murine pancreatitis.Scientific reports · 2025Article
- TheBiomolecules · 2025Review
- Identification of Potential Hub Genes Related to Acute Pancreatitis and Chronic Pancreatitis via Integrated Bioinformatics Analysis and In Vitro Analysis.Molecular biotechnology · 2025Article
- Hematological and biochemical characterization of aging farm male rat strains in the national center for geriatrics and gerontology.Experimental animals · 2025Article
- DGA ameliorates severe acute pancreatitis through modulating macrophage pyroptosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Secretagogue-induced pancreatitis in mice devoid of chymotrypsin.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Krüppel-like Factor 5 Plays an Important Role in the Pathogenesis of Chronic Pancreatitis.Cancers · 2023Article
- psupertime: supervised pseudotime analysis for time-series single-cell RNA-seq data.Bioinformatics (Oxford, England) · 2022Article
- Variants in the pancreatic CUB and zona pellucida-like domains 1 (CUZD1) gene in early-onset chronic pancreatitis - A possible new susceptibility gene.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2022Article
- Targeting Endoplasmic Reticulum Stress as an Effective Treatment for Alcoholic Pancreatitis.Biomedicines · 2022Review
- Metabolic differences and differentially expressed genes between C57BL/6J and C57BL/6N mice substrains.PloS one · 2022Article
- Keratin 8 Is an Inflammation-Induced and Prognosis-Related Marker for Pancreatic Adenocarcinoma.Disease markers · 2022Article
- Substrains matter in phenotyping of C57BL/6 mice.Experimental animals · 2021Review
- Spermine-Related DNA Hypermethylation and Elevated Expression of Genes for Collagen Formation are Susceptible Factors for Chemotherapy-Induced Hand-Foot Syndrome in Chinese Colorectal Cancer Patients.Frontiers in pharmacology · 2021Article
- TheFrontiers in molecular neuroscience · 2021Article
- Loss of RE-1 silencing transcription factor accelerates exocrine damage from pancreatic injury.Cell death & disease · 2020Article
- Pancreatitis is an FGF21-deficient state that is corrected by replacement therapy.Science translational medicine · 2020Article
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5 authors at 3 institutions in 3 countries.
Funding
Abstract
A frequently used experimental model of chronic pancreatitis (CP) recapitulating human disease is repeated injection of cerulein into mice. C57BL/6 is the most commonly used inbred mouse strain for biomedical research, but widespread demand has led to generation of several substrains with subtly different phenotypes. In this study, two common substrains, C57BL/6J and C57BL/6NHsd, exhibited different degrees of CP, with C57BL/6J being more susceptible to repetitive cerulein-induced CP as assessed by pancreatic atrophy, pancreatic morphological changes, and fibrosis. We hypothesized that the deficiency of nicotinamide nucleotide transhydrogenase (NNT) protein in C57BL/6J is responsible for the more severe C57BL/6J phenotype but the parameters of CP in NNT-expressing transgenic mice generated on a C57BL6/J background do not differ with those of wild-type C57BL/6J. The highly similar genetic backgrounds but different CP phenotypes of these two substrains presents a unique opportunity to discover genes important in pathogenesis of CP. We therefore performed whole mouse genome Affymetrix microarray analysis of pancreatic gene expression of C57BL/6J and C57BL/6NHsd before and after induction of CP. Genes with differentially regulated expression between the two substrains that might be candidates in CP progression included Mmp7, Pcolce2, Itih4, Wdfy1, and Vtn. We also identified several genes associated with development of CP in both substrains, including RIKEN cDNA 1810009J06 gene (trypsinogen 5), Ccl8, and Ccl6.
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