Evidence map›Paper›PMID 30372685›Full record

ArticleJournal of Alzheimer's disease : JAD2018

Glia Maturation Factor and Mast Cell-Dependent Expression of Inflammatory Mediators and Proteinase Activated Receptor-2 in Neuroinflammation.

Duraisamy Kempuraj, Govindhasamy Pushpavathi Selvakumar, Ramasamy Thangavel, Mohammad Ejaz Ahmed, Smita Zaheer, Keerthana Kuppamma Kumar, Anudeep Yelam, Harleen Kaur, Iuliia Dubova, Sudhanshu P Raikwar and 2 more

Open access · greenAbstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  11. Decoding Mast Cell-Microglia Communication in Neurodegenerative Diseases.International journal of molecular sciences · 2021
    Review
  12. Article
  13. Article
  14. Review
  15. Brain Injury-Mediated Neuroinflammatory Response and Alzheimer's Disease.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2020
    Review
  16. Article
  17. Next Generation Precision Medicine: CRISPR-mediated Genome Editing for the Treatment of Neurodegenerative Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019
    Review
  18. Article
  19. 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

12 authors at 3 institutions in 1 country.

Duraisamy KempurajHarry S. Truman Memorial Veterans Hospital, U.S. Department of Veterans Affairs, Columbia, MO, USA.
Govindhasamy Pushpavathi SelvakumarHarry S. Truman Memorial Veterans Hospital, U.S. Department of Veterans Affairs, Columbia, MO, USA.
Ramasamy ThangavelHarry S. Truman Memorial Veterans Hospital, U.S. Department of Veterans Affairs, Columbia, MO, USA.
Mohammad Ejaz AhmedHarry S. Truman Memorial Veterans Hospital, U.S. Department of Veterans Affairs, Columbia, MO, USA.
Smita ZaheerDepartment of Neurology, and the Center for Translational Neuroscience, School of Medicine, University of Missouri, Columbia, MO, USA.
Keerthana Kuppamma KumarDepartment of Neurology, and the Center for Translational Neuroscience, School of Medicine, University of Missouri, Columbia, MO, USA.
Anudeep YelamDepartment of Neurology, and the Center for Translational Neuroscience, School of Medicine, University of Missouri, Columbia, MO, USA.
Harleen KaurDepartment of Neurology, and the Center for Translational Neuroscience, School of Medicine, University of Missouri, Columbia, MO, USA.
Iuliia DubovaDepartment of Neurology, and the Center for Translational Neuroscience, School of Medicine, University of Missouri, Columbia, MO, USA.
Sudhanshu P RaikwarHarry S. Truman Memorial Veterans Hospital, U.S. Department of Veterans Affairs, Columbia, MO, USA.
Shankar S IyerHarry S. Truman Memorial Veterans Hospital, U.S. Department of Veterans Affairs, Columbia, MO, USA.
Asgar ZaheerHarry S. Truman Memorial Veterans Hospital, U.S. Department of Veterans Affairs, Columbia, MO, USA.
University of Missouri · USHarry S. Truman Memorial Veterans' Hospital · USUnited States Department of Veterans Affairs · US

Funding

GMF-dependent neuroinflammation and neurodegenerationR01NS073670 · NINDS · UNIVERSITY OF MISSOURI-COLUMBIA · PI ZAHEER, ASGAR · 2011 to 2015
$1.6M
Therapeutic potential of GMF suppresssion in inflammation and neurodegenerationR01AG048205 · NIA · UNIVERSITY OF MISSOURI-COLUMBIA · PI ZAHEER, ASGAR · 2015 to 2019
$1.6M
Glia maturation factor dependent mast cell activation in Parkinson's diseaseI01BX002477 · VA · IOWA CITY VA MEDICAL CENTER · PI ZAHEER, ASGAR · 2015 to 2017
–
BLRD VA I01 BX002477NIA NIH HHS R01 AG048205NINDS NIH HHS R01 NS073670
6 · The paper itself

Abstract

Parkinson's disease (PD) is characterized by the presence of inflammation-mediated dopaminergic neurodegeneration in the substantia nigra. Inflammatory mediators from activated microglia, astrocytes, neurons, T-cells and mast cells mediate neuroinflammation and neurodegeneration. Administration of neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induces PD like motor deficits in rodents. 1-methyl-4-phenylpyridinium (MPP+), a toxic metabolite of MPTP activates glial cells, neurons and mast cells to release neuroinflammatory mediators. Glia maturation factor (GMF), mast cells and proteinase activated receptor-2 (PAR-2) are implicated in neuroinflammation. Alpha-synuclein which induces neurodegeneration increases PAR-2 expression in the brain. However, the exact mechanisms are not yet understood. In this study, we quantified inflammatory mediators in the brains of MPTP-administered wild type (Wt), GMF-knockout (GMF-KO), and mast cell knockout (MC-KO) mice. Additionally, we analyzed the effect of MPP+, GMF, and mast cell proteases on PAR-2 expression in astrocytes and neurons in vitro. Results show that the levels of interleukin-1beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and the chemokine (C-C motif) ligand 2 (CCL2) were lesser in the brains of GMF-KO mice and MC-KO mice when compared to Wt mice brain after MPTP administration. Incubation of astrocytes and neurons with MPP+, GMF, and mouse mast cell protease-6 (MMCP-6) and MMCP-7 increased the expression of PAR-2. Our studies show that the absence of mast cells and GMF reduce the expression of neuroinflammatory mediators in the brain. We conclude that GMF along with mast cell interactions with glial cells and neurons during neuroinflammation can be explored as a new therapeutic target for PD and other neuroinflammatory disorders.

Indexed as

AnimalsAstrocytesBrainCells, CulturedChemokine CCL2ChymasesGlia Maturation FactorInflammation MediatorsInterleukin-1betaMast CellsMiceMice, KnockoutNeuronsParkinsonian DisordersReceptor, PAR-2Tumor Necrosis Factor-alphaChemokine CCL2ChymasesF2rl1 protein, mouseGlia Maturation FactorInflammation MediatorsInterleukin-1betaReceptor, PAR-2Tumor Necrosis Factor-alphaAstrocytescytokinesglia maturation factormast cellsmouse mast cell proteasesPAR-2Parkinson’s disease

Identifiers

PMID30372685
PMCPMC6334644
OpenAlexW2898608757

What OpenQuestion holds

Textmetadata
LicenceTDM
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.