ArticleDevelopment (Cambridge, England)2017
PDGF controls contact inhibition of locomotion by regulating N-cadherin during neural crest migration.
Article in Development (Cambridge, England), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 70 citations in OpenAlex.
- Identification of 4 novel human ocular coloboma genes ANK3, BMPR1B, PDGFRA, and CDH4 through evolutionary conserved vertebrate gene analysis.Genetics in medicine : official journal of the American College of Medical Genetics · 2022Pooled it
- Conservation of Epithelial-to-Mesenchymal Transition Process in Neural Crest Cells and Metastatic Cancer.Cells, tissues, organs · 2021Pooled it
- Nf2/FGFR1/AKT axis directs cranial neural crest-derived skull morphogenesis via collagen synthesis and trafficking.JCI insight · 2025Article
- Pdgfab/Pdgfra-mediated chemoattraction guides the migration of sclerotome-derived fibroblast precursors in zebrafish.PLoS biology · 2025Article
- Article
- EZH2 controls epicardial cell migration during heart development.Life science alliance · 2023Article
- The myocardium utilizes Pdgfra-PI3K signaling to steer towards the midline during heart tube formation.bioRxiv : the preprint server for biology · 2023Article
- Time to go: neural crest cell epithelial-to-mesenchymal transition.Development (Cambridge, England) · 2022Review
- The mechanosensitive channel Piezo1 cooperates with semaphorins to control neural crest migration.Development (Cambridge, England) · 2021Article
- Profiling of Human Neural Crest Chemoattractant Activity as a Replacement of Fetal Bovine Serum for In Vitro Chemotaxis Assays.International journal of molecular sciences · 2021Article
- PDGFRα: Expression and Function during Mitral Valve Morphogenesis.Journal of cardiovascular development and disease · 2021Article
- The RNA helicase DDX3 induces neural crest by promoting AKT activity.Development (Cambridge, England) · 2021Article
- Non-junctional role of Cadherin3 in cell migration and contact inhibition of locomotion via domain-dependent, opposing regulation of Rac1.Scientific reports · 2020Article
- Epithelial-to-mesenchymal transition and different migration strategies as viewed from the neural crest.Current opinion in cell biology · 2020Review
- The extracellular matrix in development.Development (Cambridge, England) · 2020Review
- The road best traveled: Neural crest migration upon the extracellular matrix.Seminars in cell & developmental biology · 2020Review
- Exposure to small molecule cocktails allows induction of neural crest lineage cells from human adipose-derived mesenchymal stem cells.PloS one · 2020Article
- Insights Into the Early Gene Regulatory Network Controlling Neural Crest and Placode Fate Choices at the Neural Border.Frontiers in physiology · 2020Review
- Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
A fundamental property of neural crest (NC) migration is contact inhibition of locomotion (CIL), a process by which cells change their direction of migration upon cell contact. CIL has been proven to be essential for NC migration in amphibians and zebrafish by controlling cell polarity in a cell contact-dependent manner. Cell contact during CIL requires the participation of the cell adhesion molecule N-cadherin, which starts to be expressed by NC cells as a consequence of the switch between E- and N-cadherins during epithelial-to-mesenchymal transition (EMT). However, the mechanism that controls the upregulation of N-cadherin remains unknown. Here, we show that platelet-derived growth factor receptor alpha (PDGFRα) and its ligand platelet-derived growth factor A (PDGF-A) are co-expressed in migrating cranial NC. Inhibition of PDGF-A/PDGFRα blocks NC migration by inhibiting N-cadherin and, consequently, impairing CIL. Moreover, we identify phosphatidylinositol-3-kinase (PI3K)/AKT as a downstream effector of the PDGFRα cellular response during CIL. Our results lead us to propose PDGF-A/PDGFRα signalling as a tissue-autonomous regulator of CIL by controlling N-cadherin upregulation during EMT. Finally, we show that once NC cells have undergone EMT, the same PDGF-A/PDGFRα works as an NC chemoattractant, guiding their directional migration.
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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.