Evidence map›Paper›PMID 32705814›Full record

ArticleBrain and behavior2020

Extracellular matrix proteins are time-dependent and regional-specific markers in experimental diffuse brain injury.

Daniel R Griffiths, Taylor M Jenkins, Caroline P Addington, Sarah E Stabenfeldt, Jonathan Lifshitz

Open access · goldAbstract read
In one paragraph

Article in Brain and behavior, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
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  12. Tenascin-C induction exacerbates post-stroke brain damage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022
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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 3 institutions in 1 country.

Daniel R GriffithsBARROW Neurological Institute at Phoenix Children's Hospital, Phoenix, AZ, USA.ORCID 0000-0001-6558-261X
Taylor M JenkinsDepartment of Child Health, University of Arizona College of Medicine - Phoenix, Phoenix, AZ, USA.
Caroline P AddingtonSchool of Biological and Health Systems Engineering, Ira A. Fulton Schools of Engineering, Arizona State University, Tempe, AZ, USA.
Sarah E StabenfeldtSchool of Biological and Health Systems Engineering, Ira A. Fulton Schools of Engineering, Arizona State University, Tempe, AZ, USA.ORCID 0000-0003-3606-026X
Jonathan LifshitzBARROW Neurological Institute at Phoenix Children's Hospital, Phoenix, AZ, USA.ORCID 0000-0002-4398-6493
Arizona State University · USBarrow Neurological Institute · USUniversity of Arizona · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe extracellular matrix (ECM) provides structural support for neuronal, glial, and vascular components of the brain, and regulates intercellular signaling required for cellular morphogenesis, differentiation and homeostasis. We hypothesize that the pathophysiology of diffuse brain injury impacts the ECM in a multi-dimensional way across brain regions and over time, which could facilitate damage and repair processes.

methodsExperimental diffuse TBI was induced in male Sprague-Dawley rats (325-375 g) by midline fluid percussion injury (FPI); uninjured sham rats serve as controls. Tissue from the cortex, thalamus, and hippocampus was collected at 15 min, 1, 2, 6, and 18 hr postinjury as well as 1, 3, 7, and 14 days postinjury. All samples were quantified by Western blot for glycoproteins: fibronectin, laminin, reelin, and tenascin-C. Band intensities were normalized to sham and relative to β-actin.

resultsIn the cortex, fibronectin decreased significantly at 15 min, 1 hr, and 2 hr postinjury, while tenascin-C decreased significantly at 7 and 14 days postinjury. In the thalamus, reelin decreased significantly at 2 hr, 3 and 14 days postinjury. In the hippocampus, tenascin-C increased significantly at 15 min and 7 days postinjury.

conclusionAcute changes in the levels of these glycoproteins suggest involvement in circuit dismantling, whereas postacute levels may indicate a restorative or regenerative response associated with recovery from TBI.

Indexed as

Brain InjuriesBrain Injuries, DiffuseAnimalsDisease Models, AnimalExtracellular Matrix ProteinsMaleRatsRats, Sprague-DawleyReelin ProteinThalamusExtracellular Matrix ProteinsReelin ProteinReln protein, ratextracellular matrixprimary somatosensory barrel cortexproteinS1BFtraumatic brain injuryventral posterior medialventral posterior medial thalamus

Identifiers

PMID32705814
PMCPMC7507085
OpenAlexW3043939602

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.