Evidence map›Paper›PMID 11331362›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001

Semaphorin 3A-vascular endothelial growth factor-165 balance mediates migration and apoptosis of neural progenitor cells by the recruitment of shared receptor.

D Bagnard, C Vaillant, S T Khuth, N Dufay, M Lohrum, A W Puschel, M F Belin, J Bolz, N Thomasset

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
7.4field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

70 citing papers in PubMed, 228 citations in OpenAlex.

  1. Neonatal diethylstilbestrol exposure disrupts uterine epithelial apical-basal polarity and partial EMT state.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  2. Review
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  4. Article
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  7. Semaphorins in Adult Nervous System Plasticity and Disease.Frontiers in synaptic neuroscience · 2021
    Review
  8. Article
  9. Article
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  12. Vascularization Strategies for Peripheral Nerve Tissue Engineering.Anatomical record (Hoboken, N.J. : 2007) · 2018
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

10 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 2 countries.

D BagnardInstitut National de la Santé et de la Recherche Médicale U433, Neurobiologie Experimentale et Physiopathologie, Faculté de Médecine Laënnec, 69372 Lyon cedex 08, France.
C Vaillant
S T Khuth
N Dufay
M Lohrum
A W Puschel
M F Belin
J Bolz
N Thomasset
Inserm · FRInstitut de Neurobiologie de la Méditerranée · FRMax Planck Institute for Brain Research · DEFriedrich Schiller University Jena · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The dynamic and coordinated interaction between cells and their microenvironment controls cell migration, proliferation, and apoptosis, mediated by different cell surface molecules. We have studied the response of a neuroectodermal progenitor cell line, Dev, to a guidance molecule, semaphorin 3A (Sema3A), described previously as a repellent-collapsing signal for axons, and we have shown that Sema3A acts as a repellent guidance cue for migrating progenitor cells and, on prolonged application, induces apoptosis. Both repulsion and induction of cell death are mediated by neuropilin-1, the ligand-binding component of the Sema3A receptor. The vascular endothelial growth factor, VEGF165, antagonizes Sema3A-induced apoptosis and promotes cell survival, migration, and proliferation. Surprisingly, repulsion by Sema3A also depends on expression of VEGFR1, a VEGF165 receptor, expressed in Dev cells. Moreover, we found that these repulsive effects of Sema3A require tyrosine kinase activity, which can be attributed to VEGFR1. These results indicate that the balance between guidance molecules and angiogenic factors can modulate the migration, apoptosis (or survival), and proliferation of neural progenitor cells through shared receptors.

Indexed as

AntibodiesApoptosisBinding, CompetitiveCell DivisionCell LineCell MovementCell SurvivalDose-Response Relationship, DrugEndothelial Growth FactorsEnzyme InhibitorsGlycoproteinsHumansLymphokinesMedulloblastomaMicroscopy, VideoNerve Tissue ProteinsAntibodiesEndothelial Growth FactorsEnzyme InhibitorsGlycoproteinsLymphokinesNerve Tissue ProteinsNeuropilin-1Proto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesReceptors, Cell SurfaceReceptors, Growth FactorReceptors, Vascular Endothelial Growth FactorRNA, MessengerSemaphorin-3AVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth FactorsVEGFA protein, human

Identifiers

PMID11331362
PMCPMC6762465
OpenAlexW1927563061

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.