Evidence map›Paper›PMID 32684835›Full record

ArticleMediators of inflammation2020

Mast Cell Activation, Neuroinflammation, and Tight Junction Protein Derangement in Acute Traumatic Brain Injury.

Duraisamy Kempuraj, Mohammad Ejaz Ahmed, Govindhasamy Pushpavathi Selvakumar, Ramasamy Thangavel, Sudhanshu P Raikwar, Smita A Zaheer, Shankar S Iyer, Casey Burton, Donald James, Asgar Zaheer

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
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  12. Potential Role of Moesin in Regulating Mast Cell Secretion.International journal of molecular sciences · 2023
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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

10 authors at 2 institutions in 1 country.

Duraisamy KempurajDepartment of Neurology, School of Medicine, University of Missouri, Columbia, MO, USA.ORCID https://orcid.org/0000-0003-1148-8681
Mohammad Ejaz AhmedDepartment of Neurology, School of Medicine, University of Missouri, Columbia, MO, USA.
Govindhasamy Pushpavathi SelvakumarDepartment of Neurology, School of Medicine, University of Missouri, Columbia, MO, USA.
Ramasamy ThangavelDepartment of Neurology, School of Medicine, University of Missouri, Columbia, MO, USA.
Sudhanshu P RaikwarDepartment of Neurology, School of Medicine, University of Missouri, Columbia, MO, USA.
Smita A ZaheerDepartment of Neurology, School of Medicine, University of Missouri, Columbia, MO, USA.
Shankar S IyerDepartment of Neurology, School of Medicine, University of Missouri, Columbia, MO, USA.
Casey BurtonPhelps Health, Rolla, MO, USA.
Donald JamesPhelps Health, Rolla, MO, USA.
Asgar ZaheerDepartment of Neurology, School of Medicine, University of Missouri, Columbia, MO, USA.ORCID https://orcid.org/0000-0003-3344-0371
United States Department of Veterans Affairs · USUniversity of Missouri · US

Funding

Therapeutic potential of GMF suppresssion in inflammation and neurodegenerationR01AG048205 · NIA · UNIVERSITY OF MISSOURI-COLUMBIA · PI ZAHEER, ASGAR · 2015 to 2019
$1.6M
NIA NIH HHS R01 AG048205
6 · The paper itself

Abstract

Traumatic brain injury (TBI) is one of the major health problems worldwide that causes death or permanent disability through primary and secondary damages in the brain. TBI causes primary brain damage and activates glial cells and immune and inflammatory cells, including mast cells in the brain associated with neuroinflammatory responses that cause secondary brain damage. Though the survival rate and the neurological deficiencies have shown significant improvement in many TBI patients with newer therapeutic options, the underlying pathophysiology of TBI-mediated neuroinflammation, neurodegeneration, and cognitive dysfunctions is understudied. In this study, we analyzed mast cells and neuroinflammation in weight drop-induced TBI. We analyzed mast cell activation by toluidine blue staining, serum chemokine C-C motif ligand 2 (CCL2) level by enzyme-linked immunosorbent assay (ELISA), and proteinase-activated receptor-2 (PAR-2), a mast cell and inflammation-associated protein, vascular endothelial growth factor receptor 2 (VEGFR2), and blood-brain barrier tight junction-associated claudin 5 and Zonula occludens-1 (ZO-1) protein expression in the brains of TBI mice. Mast cell activation and its numbers increased in the brains of 24 h and 72 h TBI when compared with sham control brains without TBI. Mouse brains after TBI show increased CCL2, PAR-2, and VEGFR2 expression and derangement of claudin 5 and ZO-1 expression as compared with sham control brains. TBI can cause mast cell activation, neuroinflammation, and derangement of tight junction proteins associated with increased BBB permeability. We suggest that inhibition of mast cell activation can suppress neuroimmune responses and glial cell activation-associated neuroinflammation and neurodegeneration in TBI.

Indexed as

AnimalsBlood-Brain BarrierBrainBrain InjuriesBrain Injuries, TraumaticChemokine CCL2Claudin-5Disease Models, AnimalMaleMast CellsMiceMice, Inbred C57BLReceptor, PAR-2Tight Junction ProteinsVascular Endothelial Growth Factor Receptor-2Zonula Occludens-1 ProteinChemokine CCL2Claudin-5Cldn5 protein, mouseF2rl1 protein, mouseKdr protein, mouseReceptor, PAR-2Tight Junction ProteinsTjp1 protein, mouseVascular Endothelial Growth Factor Receptor-2Zonula Occludens-1 Protein

Identifiers

PMID32684835
PMCPMC7333064
OpenAlexW3038076142

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.