Evidence map›Paper›PMID 18627255›Full record

ArticleJournal of neurotrauma2008

Agrin expression during synaptogenesis induced by traumatic brain injury.

M Cristina Falo, Thomas M Reeves, Linda L Phillips

Open access · greenAbstract read
In one paragraph

Article in Journal of neurotrauma, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

24 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. The Role of Astrocytes in the Neurorepair Process.Frontiers in cell and developmental biology · 2021
    Article
  4. Article
  5. Review
  6. Matrix metalloproteinase signals following neurotrauma are right on cue.Cellular and molecular life sciences : CMLS · 2019
    Review
  7. MMPs in learning and memory and neuropsychiatric disorders.Cellular and molecular life sciences : CMLS · 2019
    Review
  8. Article
  9. Article
  10. Extracellular matrix and traumatic brain injury.Journal of neuroscience research · 2018
    Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  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

3 authors at 2 institutions in 1 country.

M Cristina FaloDepartment of Anatomy and Neurobiology, School of Medicine, Virginia Commonwealth University Medical Center, Richmond, Virginia 23298, USA.
Thomas M Reeves
Linda L Phillips
Virginia Commonwealth University Medical Center · USVirginia Commonwealth University · US

Funding

VCU Neuroscience Center Core GrantP30NS047463 · NINDS · VIRGINIA COMMONWEALTH UNIVERSITY · PI POVLISHOCK, JOHN T · 2003 to 2013
$5.0M
Matrix Metalloproteinases and Regenerative Plasticity Following Brain InjuryR01NS044372 · NINDS · VIRGINIA COMMONWEALTH UNIVERSITY · PI PHILLIPS, LINDA L. · 2002 to 2011
$2.9M
Matrix Metalloproteinases and Regenerative Plasticity Following Brain InjuryR56NS044372 · NINDS · VIRGINIA COMMONWEALTH UNIVERSITY · PI PHILLIPS, LINDA L. · 2007 to 2007
$373k
NINDS NIH HHS NS-44372NINDS NIH HHS P30 NS-047463NINDS NIH HHS R01 NS044372
6 · The paper itself

Abstract

Interaction between extracellular matrix proteins and regulatory proteinases can mediate synaptic integrity. Previously, we documented that matrix metalloproteinase 3 (MMP-3) expression and activity increase following traumatic brain injury (TBI). We now report protein and mRNA analysis of agrin, a MMP-3 substrate, over the time course of trauma-induced synaptogenesis. Agrin expression during the successful synaptic reorganization of unilateral entorhinal cortical lesion (UEC) was compared with expression when normal synaptogenesis fails (combined fluid percussion TBI and bilateral entorhinal lesion [BEC]). We observed that agrin protein was increased in both models at 2 and 7 days postinjury, and immuohistochemical (IHC) co-localization suggested reactive astrocytes contribute to that increase. Agrin formed defined boundaries for sprouting axons along deafferented dendrites in the UEC, but failed to do so after combined insult. Similarly, Western blot analysis revealed greater increase in UEC agrin protein relative to the combined TBI+BEC model. Both models showed increased agrin transcription at 7 days postinjury and mRNA normalization by 15 days. Attenuation of synaptic pathology with the NMDA antagonist MK-801 reduced 7-day UEC agrin transcript to a level not different from unlesioned controls. By contrast, MK-801 in the combined insult failed to significantly change 7-day agrin transcript, mRNA levels remaining elevated over uninjured sham cases. Together, these results suggest that agrin plays an important role in the sprouting phase of reactive synaptogenesis, and that both its expression and distribution are correlated with extent of successful recovery after TBI. Further, when pathogenic conditions which induce synaptic plasticity are reduced, increase in agrin mRNA is attenuated.

Indexed as

AgrinAnimalsBrain InjuriesDenervationDisease Models, AnimalDizocilpine MaleateEntorhinal CortexExcitatory Amino Acid AntagonistsExtracellular MatrixGene Expression RegulationMaleMatrix Metalloproteinase 3Nerve RegenerationNeuronal PlasticityNeuroprotective AgentsPresynaptic TerminalsAgrinDizocilpine MaleateExcitatory Amino Acid AntagonistsMatrix Metalloproteinase 3Neuroprotective AgentsReceptors, N-Methyl-D-AspartateRNA, Messenger

Identifiers

PMID18627255
PMCPMC2946878
OpenAlexW2091415034

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.