Evidence map›Paper›PMID 19053061›Full record

ArticleGlia2009

Disruption of laminin in the peripheral nervous system impedes nonmyelinating Schwann cell development and impairs nociceptive sensory function.

Wei-Ming Yu, Huaxu Yu, Zu-Lin Chen, Sidney Strickland

Abstract read
In one paragraph

Article in Glia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.6field-weighted citation impact, top 39% 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

19 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Review
  3. Drosophila glia take shape to sculpt the nervous system.Current opinion in neurobiology · 2023
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Accumulation of Laminin Monomers in Drosophila Glia Leads to Glial Endoplasmic Reticulum Stress and Disrupted Larval Locomotion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  13. Article
  14. Article
  15. Article
  16. The RNA-binding protein human antigen R controls global changes in gene expression during Schwann cell development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  17. Article
  18. Article
  19. 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

4 authors at 1 institution in 1 country.

Wei-Ming YuLaboratory of Neurobiology and Genetics, The Rockefeller University, New York, NY, USA.
Huaxu Yu
Zu-Lin Chen
Sidney Strickland
Rockefeller University · US

Funding

Role of Laminin gamma1 in the Peripheral Nervous SystemR01NS038472 · NINDS · STATE UNIVERSITY NEW YORK STONY BROOK · PI STRICKLAND, SIDNEY · 1999 to 2007
$2.8M
TISSUE PLASMINOGEN ACTIVATOR AND NEURONAL DEGENERATIONR01NS035704 · NINDS · STATE UNIVERSITY NEW YORK STONY BROOK · PI STRICKLAND, SIDNEY · 1997 to 2004
$2.1M
NINDS NIH HHS NS 035704NINDS NIH HHS NS 038472NINDS NIH HHS R01 NS035704NINDS NIH HHS R01 NS038472
6 · The paper itself

Abstract

The mechanisms controlling the differentiation of immature Schwann cells (SCs) into nonmyelinating SCs is not known. Laminins are extracellular matrix proteins critical for myelinating SC differentiation, but their roles in nonmyelinating SC development have not been established. Here, we show that the peripheral nerves of mutant mice with laminin-deficient SCs do not form Remak bundles, which consist of a single nonmyelinating SC interacting with multiple unmyelinated axons. These mutant nerves show aberrant L1 and neural cell adhesion molecule (N-CAM) expression pattern during development. The homophilic and heterophilic interactions of N-CAM are also impaired in the mutant nerves. Other molecular markers for nonmyelinating SCs, including Egr-1, glial fibrillary acidic protein, and AN2/NG2, are all absent in adult mutant nerves. Analysis of expression of SC lineage markers demonstrates that nonmyelinating SCs do not develop in mutant nerves. Additionally, mutant mice are insensitive to heat stimuli and show a decreased number of C-fiber sensory neurons, indicating reduced nociceptive sensory function. These results show that laminin participates in nonmyelinating SC development and Remak bundle formation and suggest a possible role for laminin deficiency in peripheral sensory neuropathies.

Indexed as

AnimalsAntigensCalcitonin Gene-Related PeptideChondroitin Sulfate Proteoglycan 4Gene Expression RegulationGlial Fibrillary Acidic ProteinLamininMiceMice, TransgenicMicroscopy, ImmunoelectronNerve Fibers, UnmyelinatedN-Ethylmaleimide-Sensitive ProteinsNeural Cell Adhesion MoleculesOctamer Transcription Factor-6Peripheral Nervous SystemProteoglycansAntigensCalcitonin Gene-Related PeptideChondroitin Sulfate Proteoglycan 4Glial Fibrillary Acidic ProteinLamininlaminin gamma 1N-Ethylmaleimide-Sensitive ProteinsNeural Cell Adhesion MoleculesOctamer Transcription Factor-6P2rx3 protein, mouseProteoglycansReceptors, Purinergic P2Receptors, Purinergic P2X3

Identifiers

PMID19053061
PMCPMC2670471
OpenAlexW2125561967

What OpenQuestion holds

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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.