ArticleThe Journal of clinical investigation2009
Deletion of Pten in the mouse enteric nervous system induces ganglioneuromatosis and mimics intestinal pseudoobstruction.
Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 58 citations in OpenAlex.
- Autism gene variants disrupt enteric neuron migration and cause gastrointestinal dysmotility.Nature communications · 2025Article
- Phosphatase and Tensin Homolog Inhibition in Proteolipid Protein 1-Expressing Cells Stimulates Neurogenesis and Gliogenesis in the Postnatal Enteric Nervous System.Biomolecules · 2024Article
- Differences in enteric neuronal density in the NSE-Noggin mouse model across institutes.Scientific reports · 2024Article
- A Bi-Institutional Study of Gastrointestinal and Hepatic Manifestations in Children WithGastro hep advances · 2024Article
- Stabilization of β-catenin promotes melanocyte specification at the expense of the Schwann cell lineage.Development (Cambridge, England) · 2022Article
- A Case Series of Pediatric Intestinal Ganglioneuromatosis With Novel Phenotypic and Genotypic Profile.Frontiers in medicine · 2022Article
- BRN2 is a non-canonical melanoma tumor-suppressor.Nature communications · 2021Article
- NDRG2 is expressed on enteric glia and altered in conditions of inflammation and oxygen glucose deprivation/reoxygenation.Journal of molecular histology · 2021Article
- Ganglioneuromas are driven by activated AKT and can be therapeutically targeted with mTOR inhibitors.The Journal of experimental medicine · 2020Article
- Akt phosphorylation of neuronal nitric oxide synthase regulates gastrointestinal motility in mouse ileum.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- LKB1 specifies neural crest cell fates through pyruvate-alanine cycling.Science advances · 2019Article
- Loss of Tbx3 in murine neural crest reduces enteric glia and causes cleft palate, but does not influence heart development or bowel transit.Developmental biology · 2018Article
- Filamentous Aggregation of Sequestosome-1/p62 in Brain Neurons and Neuroepithelial Cells upon Tyr-Cre-Mediated Deletion of the Autophagy Gene Atg7.Molecular neurobiology · 2018Article
- Development of the Enteric Nervous System: A Genetic Guide to the Perplexed.Gastroenterology · 2018Article
- Enteric nervous system development: A crest cell's journey from neural tube to colon.Seminars in cell & developmental biology · 2017Review
- Adult enteric nervous system in health is maintained by a dynamic balance between neuronal apoptosis and neurogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- White paper on guidelines concerning enteric nervous system stem cell therapy for enteric neuropathies.Developmental biology · 2016Review
- Mouse models of Hirschsprung disease and other developmental disorders of the enteric nervous system: Old and new players.Developmental biology · 2016Review
- Gene-environment interactions and the enteric nervous system: Neural plasticity and Hirschsprung disease prevention.Developmental biology · 2016Review
- An unusual case of Cowden syndrome associated with ganglioneuromatous polyposis.Hereditary cancer in clinical practice · 2016Article
Corrections and comments
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Authors and funding
6 authors at 6 institutions in 1 country.
Funding
Abstract
Intestinal ganglioneuromatosis is a benign proliferation of nerve ganglion cells, nerve fibers, and supporting cells of the enteric nervous system (ENS) that can result in abnormally large enteric neuronal cells (ENCs) in the myenteric plexus and chronic intestinal pseudoobstruction (CIPO). As phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is a phosphatase that is critical for controlling cell growth, proliferation, and death, we investigated the role of PTEN in the ENS by generating mice with an embryonic, ENC-selective deletion within the Pten locus. Mutant mice died 2 to 3 weeks after birth, with clinical signs of CIPO and hyperplasia and hypertrophy of ENCs resulting from increased activity of the PI3K/PTEN-AKT-S6K signaling pathway. Further analysis revealed that PTEN was only expressed in developing mouse embryonic ENCs from E15.5 and that the rate of ENC proliferation decreased once PTEN was expressed. Specific deletion of the Pten gene in ENCs therefore induced hyperplasia and hypertrophy in the later stages of embryogenesis. This phenotype was reversed by administration of a pharmacological inhibitor of AKT. In some human ganglioneuromatosis forms of CIPO, PTEN expression was found to be abnormally low and S6 phosphorylation increased. Our study thus reveals that loss of PTEN disrupts development of the ENS and identifies the PI3K/PTEN-AKT-S6K signaling pathway as a potential therapeutic target for ganglioneuromatosis forms of CIPO.
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