ArticleScientific reports2016
Endothelin-3 stimulates cell adhesion and cooperates with β1-integrins during enteric nervous system ontogenesis.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Endothelin-3 and T-type CaNature communications · 2026Article
- Aberrant Expressions ofCurrent pediatric reviews · 2026Article
- Laminin Receptors in Peripheral Tissues: Functions Revealed by Analysis of Knockout Mice.The American journal of pathology · 2025Review
- Cecal growth factors promote enteric neurosphere formation and hindgut colonization in the avian model.Frontiers in cell and developmental biology · 2025Article
- Endothelin 3/EDNRB signaling induces thermogenic differentiation of white adipose tissue.Nature communications · 2024Article
- Endothelin signaling in development.Development (Cambridge, England) · 2023Review
- Roles of Enteric Neural Stem Cell Niche and Enteric Nervous System Development in Hirschsprung Disease.International journal of molecular sciences · 2021Review
- Review
- The road best traveled: Neural crest migration upon the extracellular matrix.Seminars in cell & developmental biology · 2020Review
- Decreased expression of β1 integrin in enteric neural crest cells of the endothelin receptor B null mouse model.Pediatric surgery international · 2020Article
- Collagen 18 and agrin are secreted by neural crest cells to remodel their microenvironment and regulate their migration during enteric nervous system development.Development (Cambridge, England) · 2018Article
- The effect of laminin-1 on enteric neural crest-derived cell migration in the Hirschsprung's disease mouse model.Pediatric surgery international · 2018Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelin-3 (EDN3) and β1-integrins are required for the colonization of the embryonic gut by enteric neural crest cells (ENCCs) to form the enteric nervous system (ENS). β1-integrin-null ENCCs exhibit migratory defects in a region of the gut enriched in EDN3 and in specific extracellular matrix (ECM) proteins. We investigated the putative role of EDN3 on ENCC adhesion properties and its functional interaction with β1-integrins during ENS development. We show that EDN3 stimulates ENCC adhesion to various ECM components in vitro. It induces rapid changes in ENCC shape and protrusion dynamics favouring sustained growth and stabilization of lamellipodia, a process coincident with the increase in the number of focal adhesions and activated β1-integrins. In vivo studies and ex-vivo live imaging revealed that double mutants for Itgb1 and Edn3 displayed a more severe enteric phenotype than either of the single mutants demonstrated by alteration of the ENS network due to severe migratory defects of mutant ENCCs taking place early during the ENS development. Altogether, our results highlight the interplay between the EDN3 and β1-integrin signalling pathways during ENS ontogenesis and the role of EDN3 in ENCC adhesion.
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