Evidence map›Paper›PMID 16971524›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006

Stromal-derived factor-1 (CXCL12) regulates laminar position of Cajal-Retzius cells in normal and dysplastic brains.

Mercedes F Paredes, Guangnan Li, Omri Berger, Scott C Baraban, Samuel J Pleasure

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.1field-weighted citation impact, top 7% 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

55 citing papers in PubMed, 130 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Meninges: A Widespread Niche of Neural Progenitors for the Brain.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2021
    Review
  10. Review
  11. Article
  12. Developmental biology of the meninges.Genesis (New York, N.Y. : 2000) · 2019
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article
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

5 authors at 1 institution in 1 country.

Mercedes F ParedesDepartment of Neurosurgery, University of California, San Francisco, California 94143, USA.
Guangnan Li
Omri Berger
Scott C Baraban
Samuel J Pleasure
University of California, San Francisco · US

Funding

Epileptogenesis in the Malformed BrainR01NS040272 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BARABAN, SCOTT C · 2001 to 2013
$3.5M
Wnt Signaling in Hippocampal and Neocortical DevelopmentK02MH074958 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PLEASURE, SAMUEL JEREMY · 2005 to 2009
$569k
NIMH NIH HHS K02 MH074958NINDS NIH HHS R01 NS040272NINDS NIH HHS R01 NS40272
6 · The paper itself

Abstract

Normal brain development requires a series of highly complex and interrelated steps. This process presents many opportunities for errors to occur, which could result in developmental defects in the brain, clinically referred to as malformations of cortical development. The marginal zone and Cajal-Retzius cells are key players in cortical development and are established early, yet there is little understanding of the factors resulting in the disruption of the marginal zone in many types of cortical malformation syndromes. We showed previously that treatment with methylazoxymethanol in rats causes marginal zone dysplasia with displacement of Cajal-Retzius cells to deeper cortical layers. Here we establish that loss of activity of the chemokine stromal-derived factor-1 (SDF1) (CXCL12), which is expressed by the leptomeninges, is necessary and sufficient to cause marginal zone disorganization in this widely used teratogenic animal model. We also found that mice with mutations in the main receptor for SDF1 (CXCR4) have Cajal-Retzius cells displaced to deeper cortical layers. Furthermore, by inhibiting SDF1 signaling in utero by intraventricular injection of a receptor antagonist, we establish that SDF1 signaling is required for the maintenance of Cajal-Retzius cell position in the marginal zone during normal cortical development. Our data imply that cortical layering is not a static process, but rather requires input from locally produced molecular cues for maintenance, and that complex syndromes of cortical malformation as a result of environmental insults may still be amenable to explanation by interruption of specific molecular signaling pathways.

Indexed as

AnimalsCell DifferentiationCell MovementCerebral CortexChemokine CXCL12Chemokines, CXCDisease Models, AnimalMethylazoxymethanol AcetateNervous System MalformationsNeuronsRatsRats, Sprague-DawleyReceptors, CXCR4Stem CellsTeratogensChemokine CXCL12Chemokines, CXCCxcr4 protein, ratmethylazoxymethanolMethylazoxymethanol AcetateReceptors, CXCR4Teratogens

Identifiers

PMID16971524
PMCPMC2133346
OpenAlexW2065414392

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.