ArticleScientific reports2020
Semaphorin 3A controls enteric neuron connectivity and is inversely associated with synapsin 1 expression in Hirschsprung disease.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Time-resolved morphological and transcriptomic characterization of early enteric neuron subtype emergence in chick.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Inflammation rewires the enteric nervous system through neurogenic monocyte recruitment.The Journal of experimental medicine · 2026Article
- Glycosaminoglycan sugar side chains on perineuronal nets in the fastigial nucleus regulate motor skills.iScience · 2025Article
- Contribution of neuroligin and neurexin alternative splicing to the establishment of enteric neuronal synaptic specificity.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- The regulation of enteric neuron connectivity by semaphorin 5A is affected by the autism-associated S956G missense mutation.iScience · 2024Article
- RET enhancer haplotype-dependent remodeling of the human fetal gut development program.PLoS genetics · 2023Article
- A functional network of highly pure enteric neurons in a dish.Frontiers in neuroscience · 2022Article
- Persistent bowel dysfunction after surgery for Hirschsprung's disease: A neuropathological perspective.World journal of gastrointestinal surgery · 2021Review
- The bright side of fibroblasts: molecular signature and regenerative cues in major organs.NPJ Regenerative medicine · 2021Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Most of the gut functions are controlled by the enteric nervous system (ENS), a complex network of enteric neurons located throughout the wall of the gastrointestinal tract. The formation of ENS connectivity during the perinatal period critically underlies the establishment of gastrointestinal motility, but the factors involved in this maturation process remain poorly characterized. Here, we examined the role of Semaphorin 3A (Sema3A) on ENS maturation and its potential implication in Hirschsprung disease (HSCR), a developmental disorder of the ENS with impaired colonic motility. We found that Sema3A and its receptor Neuropilin 1 (NRP1) are expressed in the rat gut during the early postnatal period. At the cellular level, NRP1 is expressed by enteric neurons, where it is particularly enriched at growth areas of developing axons. Treatment of primary ENS cultures and gut explants with Sema3A restricts axon elongation and synapse formation. Comparison of the ganglionic colon of HSCR patients to the colon of patients with anorectal malformation shows reduced expression of the synaptic molecule synapsin 1 in HSCR, which is inversely correlated with Sema3A expression. Our study identifies Sema3A as a critical regulator of ENS connectivity and provides a link between altered ENS connectivity and HSCR.
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