Evidence map›Paper›PMID 25740503›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015

β1-Integrin alters ependymal stem cell BMP receptor localization and attenuates astrogliosis after spinal cord injury.

Hilary A North, Liuliu Pan, Tammy L McGuire, Sarah Brooker, John A Kessler

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.8field-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

26 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
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  8. Review
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  11. Bone morphogenic protein signaling in spinal cord injury.Neuroimmunology and neuroinflammation · 2021
    Article
  12. Article
  13. Article
  14. Article
  15. Wnt/β-catenin signaling regulates ependymal cell development and adult homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  16. Article
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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.

Hilary A NorthDepartment of Neurology, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611 h.north.scheler@northwestern.edu.
Liuliu PanDepartment of Neurology, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611.
Tammy L McGuireDepartment of Neurology, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611.
Sarah BrookerDepartment of Neurology, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611.ORCID http://orcid.org/0000-0002-5674-3124
John A KesslerDepartment of Neurology, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611.
Northwestern University · US

Funding

Regenerative Scaffold Technologies for CNS and DiabetesR01EB003806 · NIBIB · NORTHWESTERN UNIVERSITY AT CHICAGO · PI STUPP, SAMUEL I · 2004 to 2015
$10.7M
REGULATION OF NEUROTRANSMITTER METABOLISMR01NS020778 · NINDS · YESHIVA UNIVERSITY · PI KESSLER, JOHN A · 1985 to 2014
$4.6M
NIBIB NIH HHS R01 EB003806NINDS NIH HHS R01 NS020778NINDS NIH HHS R01 NS20778
6 · The paper itself

Abstract

Astrogliosis after spinal cord injury (SCI) is a major impediment to functional recovery. More than half of new astrocytes generated after SCI are derived from ependymal zone stem cells (EZCs). We demonstrate that expression of β1-integrin increases in EZCs following SCI in mice. Conditional knock-out of β1-integrin increases GFAP expression and astrocytic differentiation by cultured EZCs without altering oligodendroglial or neuronal differentiation. Ablation of β1-integrin from EZCs in vivo reduced the number of EZC progeny that continued to express stem cell markers after SCI, increased the proportion of EZC progeny that differentiated into GFAP+ astrocytes, and diminished functional recovery. Loss of β1-integrin increased SMAD1/5/8 and p38 signaling, suggesting activation of BMP signaling. Coimmunoprecipitation studies demonstrated that β1-integrin directly interacts with the bone morphogenetic protein receptor subunits BMPR1a and BMPR1b. Ablation of β1-integrin reduced overall levels of BMP receptors but significantly increased partitioning of BMPR1b into lipid rafts with increased SMAD1/5/8 and p38 signaling. Thus β1-integrin expression by EZCs reduces movement of BMPR1b into lipid rafts, thereby limiting the known deleterious effects of BMPR1b signaling on glial scar formation after SCI.

Indexed as

AnimalsAstrocytesBone Morphogenetic Protein ReceptorsCell DifferentiationCells, CulturedEpendymaFemaleGlial Fibrillary Acidic ProteinGliosisIntegrin beta1MaleMiceMice, Inbred C57BLNeural Stem CellsSpinal Cord InjuriesBone Morphogenetic Protein ReceptorsGlial Fibrillary Acidic ProteinIntegrin beta1astrocyteBMPintegrinneural stem cellspinal cord injury

Identifiers

PMID25740503
PMCPMC4348179
OpenAlexW2077710901

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.