ArticleJCI insight2021
Cell differentiation is disrupted by MYO5B loss through Wnt/Notch imbalance.
Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- AP-1B Controls Several Levels of Cell Proliferation and Differentiation in Mouse Enteroids.Biology of the cell · 2026Article
- Myosin VB is critical for progenitor cell identity and function in the intestine.Stem cell reports · 2026Article
- Myosin 5b deficiency alters liver proliferation, zonation, and bile acid composition.Hepatology communications · 2026Article
- Acute tuft cell ablation in mice induces malabsorption and alterations in secretory and immune cell lineages in the small intestine.Physiological reports · 2025Article
- Is LPAR5 agonist a new treatment for microvilli inclusion disease?American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- Long-term exposure to constant light disrupts intestinal stem cells through sympathoexcitation-induced Wnt5a signaling inhibition.Gastroenterology report · 2025Article
- Alterations in cellular metabolic pathway and epithelial cell maturation induced by MYO5B defects are partially reversible by LPAR5 activation.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Modeling the cell biology of monogenetic intestinal epithelial disorders.The Journal of cell biology · 2024Review
- A purified diet affects intestinal epithelial proliferation and barrier functions through gut microbial alterations.International immunology · 2024Article
- Intestinal Tuft Cells: Morphology, Function, and Implications for Human Health.Annual review of physiology · 2024Review
- Patient-derived enteroids provide a platform for the development of therapeutic approaches in microvillus inclusion disease.The Journal of clinical investigation · 2023Article
- The genetics of monogenic intestinal epithelial disorders.Human genetics · 2023Review
- Therapy Development for Microvillus Inclusion Disease using Patient-derived Enteroids.bioRxiv : the preprint server for biology · 2023Article
- Listeria motility increases the efficiency of epithelial invasion during intestinal infection.PLoS pathogens · 2022Article
- Myosin 5b is required for proper localization of the intermicrovillar adhesion complex in the intestinal brush border.American journal of physiology. Gastrointestinal and liver physiology · 2022Article
- Applications of human organoids in the personalized treatment for digestive diseases.Signal transduction and targeted therapy · 2022Review
- Rab11FIP1-deficient mice develop spontaneous inflammation and show increased susceptibility to colon damage.American journal of physiology. Gastrointestinal and liver physiology · 2022Article
- Luminal Chemosensory Cells in the Small Intestine.Nutrients · 2021Review
- LPAR5 as a prospective therapeutic target for treating microvillus inclusion disease.Expert opinion on therapeutic targetsArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Functional loss of myosin Vb (MYO5B) induces a variety of deficits in intestinal epithelial cell function and causes a congenital diarrheal disorder, microvillus inclusion disease (MVID). The impact of MYO5B loss on differentiated cell lineage choice has not been investigated. We quantified the populations of differentiated epithelial cells in tamoxifen-induced, epithelial cell-specific MYO5B-knockout (VilCreERT2 Myo5bfl/fl) mice utilizing digital image analysis. Consistent with our RNA-sequencing data, MYO5B loss induced a reduction in tuft cells in vivo and in organoid cultures. Paneth cells were significantly increased by MYO5B deficiency along with expansion of the progenitor cell zone. We further investigated the effect of lysophosphatidic acid (LPA) signaling on epithelial cell differentiation. Intraperitoneal LPA significantly increased tuft cell populations in both control and MYO5B-knockout mice. Transcripts for Wnt ligands were significantly downregulated by MYO5B loss in intestinal epithelial cells, whereas Notch signaling molecules were unchanged. Additionally, treatment with the Notch inhibitor dibenzazepine (DBZ) restored the populations of secretory cells, suggesting that the Notch pathway is maintained in MYO5B-deficient intestine. MYO5B loss likely impairs progenitor cell differentiation in the small intestine in vivo and in vitro, partially mediated by Wnt/Notch imbalance. Notch inhibition and/or LPA treatment may represent an effective therapeutic approach for treatment of MVID.
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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.