Evidence map›Paper›PMID 30661228›Full record

ArticleNeurochemical research2019

Inflammation in Traumatic Brain Injury: Roles for Toxic A1 Astrocytes and Microglial-Astrocytic Crosstalk.

David P Q Clark, Victoria M Perreau, Sandy R Shultz, Rhys D Brady, Enie Lei, Shilpi Dixit, Juliet M Taylor, Philip M Beart, Wah Chin Boon

Abstract read
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Article in Neurochemical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
7.0field-weighted citation impact, top 3% 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

77 citing papers in PubMed, 124 citations in OpenAlex.

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17 more citing papers are in PubMed but not listed here.

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

9 authors at 3 institutions in 1 country.

David P Q ClarkThe Florey Institute of Neuroscience and Mental Health, Parkville, VIC, 3051, Australia.
Victoria M PerreauThe Florey Institute of Neuroscience and Mental Health, Parkville, VIC, 3051, Australia.
Sandy R ShultzDepartment of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, 3004, Australia.
Rhys D BradyDepartment of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, 3004, Australia.
Enie LeiThe Florey Institute of Neuroscience and Mental Health, Parkville, VIC, 3051, Australia.
Shilpi DixitThe Florey Institute of Neuroscience and Mental Health, Parkville, VIC, 3051, Australia.
Juliet M TaylorDepartment of Pharmacology & Therapeutics, University of Melbourne, Parkville, VIC, 3010, Australia.
Philip M BeartThe Florey Institute of Neuroscience and Mental Health, Parkville, VIC, 3051, Australia. philip.beart@florey.edu.au.
Wah Chin BoonThe Florey Institute of Neuroscience and Mental Health, Parkville, VIC, 3051, Australia.
Florey Institute of Neuroscience and Mental Health · AUThe Royal Melbourne Hospital · AUUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traumatic brain injury triggers neuroinflammation that may contribute to progressive neurodegeneration. We investigated patterns of recruitment of astrocytes and microglia to inflammation after brain trauma by firstly characterising expression profiles over time of marker genes following TBI, and secondly by monitoring glial morphologies reflecting inflammatory responses in a rat model of traumatic brain injury (i.e. the lateral fluid percussion injury). Gene expression profiles revealed early elevation of expression of astrocytic marker glial fibrillary acidic protein relative to microglial marker allograft inflammatory factor 1 (also known as ionized calcium-binding adapter molecule 1). Adult rat brains collected at day 7 after injury were processed for immunohistochemistry with allograft inflammatory factor 1, glial fibrillary acidic protein and complement C3 (marker of bad/disruptive astrocytic A1 phenotype). Astrocytes positive for glial fibrillary acidic protein and complement C3 were significant increased in the injured cortex and displayed more complex patterns of arbourisation with significantly increased bifurcations. Our observations suggested that traumatic brain injury changed the phenotype of microglia from a ramified appearance with long, thin, highly branched processes to a swollen amoeboid shape in the injured cortex. These findings suggest differential glial activation with astrocytes likely undergoing strategic changes in morphology and function. Whilst a detailed analysis is needed of temporal patterns of glial activation, ours is the first evidence of a role for the bad/disruptive astrocytic A1 phenotype in an open head model of traumatic brain injury.

Indexed as

AnimalsAstrocytesBrain Injuries, TraumaticCerebral CortexComplement C3EquidaeGlial Fibrillary Acidic ProteinGoatsInflammationMaleMiceMicrogliaRabbitsRats, Sprague-DawleyComplement C3Glial Fibrillary Acidic ProteinAstrocyteGlial crosstalkInflammationToxic phenotypeTraumatic brain injury

Identifiers

PMID30661228
OpenAlexW2910556324

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.