ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2010
Inducible activation of Cre recombinase in adult mice causes gastric epithelial atrophy, metaplasia, and regenerative changes in the absence of "floxed" alleles.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 71 citations in OpenAlex.
- Regulation of STK38 by autophagy governs YAP1 activity during paligenosis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Integrated single-cell transcriptomic atlas of human gastric and colorectal tissues across diverse phenotypes.Scientific data · 2026Article
- Rhubarb water extract as a promising gastroprotective agent in Tamoxifen induced parietal cell damage in female rats: a histological study.Anatomy & cell biology · 2025Article
- Sex dependent effects of GPR109A gene deletion in myeloid cells on bone development in mice.Scientific reports · 2025Article
- A Study on Potential Sources of Perineuronal Net-Associated Sema3A in Cerebellar Nuclei Reveals Toxicity of Non-Invasive AAV-Mediated Cre Expression in the Central Nervous System.International journal of molecular sciences · 2025Article
- Review
- Cardiac-Specific Expression of Cre Recombinase Leads to Age-Related Cardiac Dysfunction Associated with Tumor-like Growth of Atrial Cardiomyocyte and Ventricular Fibrosis and Ferroptosis.International journal of molecular sciences · 2023Article
- Cre toxicity in mouse models of cardiovascular physiology and disease.Nature cardiovascular research · 2022Article
- Toxic and Phenotypic Effects of AAV_Cre Used to Transduce Mesencephalic Dopaminergic Neurons.International journal of molecular sciences · 2022Article
- Cell plasticity in regeneration in the stomach and beyond.Current opinion in genetics & development · 2022Review
- Expression of Cre recombinase in chondrocytes causes abnormal craniofacial and skeletal development.Transgenic research · 2022Article
- Colonic healing requires Wnt produced by epithelium as well as Tagln+ and Acta2+ stromal cells.Development (Cambridge, England) · 2022Article
- DGCR8 deficiency impairs macrophage growth and unleashes the interferon response to mycobacteria.Life science alliance · 2021Article
- DDIT4 Licenses Only Healthy Cells to Proliferate During Injury-induced Metaplasia.Gastroenterology · 2021Article
- Disordered autonomic function during exposure to moderate heat or exercise in a mouse model of Dravet syndrome.Neurobiology of disease · 2021Article
- CORP: Using transgenic mice to study skeletal muscle physiology.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Review
- BMP Signaling in Development, Stem Cells, and Diseases of the Gastrointestinal Tract.Annual review of physiology · 2020Review
- Proliferation and Differentiation of Gastric Mucous Neck and Chief Cells During Homeostasis and Injury-induced Metaplasia.Gastroenterology · 2020Article
- Mouse Models of Human Gastric Cancer Subtypes With Stomach-Specific CreERT2-Mediated Pathway Alterations.Gastroenterology · 2019Article
- Podocyte-specific expression of Cre recombinase promotes glomerular basement membrane thickening.American journal of physiology. Renal physiology · 2019Article
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Authors and funding
3 authors at 3 institutions in 3 countries.
Funding
Abstract
The epithelium of the mammalian gastric body comprises multiple cell types replenished by a single stem cell. The adult conformation of cell lineages occurs well after birth; hence, study of genes regulating stem cell activity is facilitated by inducible systems for gene deletion. However, there is a potential pitfall involving the commonly used inducible Cre recombinase system to delete genes: we report here that induction of Cre using standard doses of tamoxifen led to marked spasmolytic polypeptide-expressing metaplasia of the stomach within days and profound atrophy of the entire epithelium with foci of hyperplasia by 2 wk even in the absence of loxP-flanked alleles. Cre induction caused genotoxicity with TdT-mediated dUTP nick-end labeling (TUNEL)-positive apoptosis (TUNEL-positive cells) and increased levels of DNA damage markers (gammaH2AX, p53, DDIT3, GADD45A). Although Cre was expressed globally by use of a chicken actin promoter, the effects were almost entirely stomach specific. Despite severe injury, a subset of mice showed near complete healing of the gastric mucosa 11-12 wk after Cre induction, suggesting substantial gastric regenerative capacity. Finally, we show that nongenotoxic doses of tamoxifen could be used to specifically delete loxP-flanked Bmpr1a, the receptor for bone morphogenetic protein 2, 4, and 7, causing antral polyps and marked antral-pyloric hyperplasia, consistent with previous reports on Bmpr1a. Together, the results show dose-dependent, potentially reversible sensitivity of the gastric mucosa to Cre genotoxicity. Thus we propose that tamoxifen induction of Cre could be used to induce genotoxic injury to study the regenerative capacity of the gastric epithelial stem cell.
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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.