ArticleDigestive diseases and sciences2018
Apical Membrane Alterations in Non-intestinal Organs in Microvillus Inclusion Disease.
Article in Digestive diseases and sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 28 citations in OpenAlex.
- The endo-lysosomal system drives lumen formation in a human epiblast model.Nature communications · 2026Article
- iPSC-based hepatic organoids reveal a heterozygous MYO5B variant as driver of intrahepatic cholestasis.Hepatology communications · 2025Article
- Microvillus Inclusion Disease Caused byJPGN reports · 2023Article
- Luminal Chemosensory Cells in the Small Intestine.Nutrients · 2021Review
- Advanced Microscopy for Liver and Gut Ultrastructural Pathology in Patients with MVID and PFIC Caused by MYO5B Mutations.Journal of clinical medicine · 2021Article
- Congenital Diarrhea and Cholestatic Liver Disease: Phenotypic Spectrum Associated with MYO5B Mutations.Journal of clinical medicine · 2021Article
- Pharmacological and Parenteral Nutrition-Based Interventions in Microvillus Inclusion Disease.Journal of clinical medicine · 2020Review
- Unequal Effects of Myosin 5B Mutations in Liver and Intestine Determine the Clinical Presentation of Low-Gamma-Glutamyltransferase Cholestasis.Hepatology (Baltimore, Md.) · 2020Review
- Weaving the Strands of Life (Human biology · 2020Review
- A Molecular Mechanism Underlying Genotype-Specific Intrahepatic Cholestasis Resulting From MYO5B Mutations.Hepatology (Baltimore, Md.) · 2020Article
- Editing Myosin VB Gene to Create Porcine Model of Microvillus Inclusion Disease, With Microvillus-Lined Inclusions and Alterations in Sodium Transporters.Gastroenterology · 2020Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
objectivesMicrovillus inclusion disease (MVID) is a severe form of neonatal diarrhea, caused mainly by mutations in MYO5B. Inactivating mutations in MYO5B causes depolarization of enterocytes in the small intestine, which gives rise to chronic, unremitting secretory diarrhea. While the pathology of the small intestine in MVID patients is well described, little is known about extraintestinal effects of MYO5B mutation.
methodsWe examined stomach, liver, pancreas, colon, and kidney in Navajo MVID patients, who share a single homozygous MYO5B-P660L (1979C>T p.Pro660Leu, exon 16). Sections were stained for markers of the apical membrane to assess polarized trafficking.
resultsNavajo MVID patients showed notable changes in H/K-ATPase-containing tubulovesicle structure in the stomach parietal cells. Colonic mucosa was morphologically normal, but did show losses in apical ezrin and Syntaxin 3. Hepatocytes in the MVID patients displayed aberrant canalicular expression of the essential transporters MRP2 and BSEP. The pancreas showed small fragmented islets and a decrease in apical ezrin in pancreatic ducts. Kidney showed normal primary cilia.
conclusionsThese findings indicate that the effects of the P660L mutation in MYO5B in Navajo MVID patients are not limited to the small intestine, but that certain tissues may be able to compensate functionally for alterations in apical trafficking.
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