Evidence map›Paper›PMID 24430624›Full record

ArticleJournal of molecular neuroscience : MN2014

Glia maturation factor deficiency suppresses 1-methyl-4-phenylpyridinium-induced oxidative stress in astrocytes.

Mohammad Moshahid Khan, Duraisamy Kempuraj, Smita Zaheer, Asgar Zaheer

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular neuroscience : MN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.4field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Frontiers in neuroscience · 2020
    Article
  6. CRISPR/Cas9 Editing of Glia Maturation Factor Regulates Mitochondrial Dynamics by Attenuation of the NRF2/HO-1 Dependent Ferritin Activation in Glial Cells.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019
    Article
  7. 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
  8. Article
  9. GMF as an Actin Network Remodeling Factor.Trends in cell biology · 2018
    Review
  10. Article
  11. Cross-Talk between Glia, Neurons and Mast Cells in Neuroinflammation Associated with Parkinson's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2018
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Co Expression ofIranian journal of parasitology
    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

4 authors at 1 institution in 1 country.

Mohammad Moshahid KhanDepartment of Neurology, University of Iowa, Iowa City, IA, 52242, USA.
Duraisamy Kempuraj
Smita Zaheer
Asgar Zaheer
University of Iowa · US

Funding

GMF-dependent neuroinflammation and neurodegenerationR01NS073670 · NINDS · UNIVERSITY OF MISSOURI-COLUMBIA · PI ZAHEER, ASGAR · 2011 to 2015
$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 BX002477NINDS NIH HHS NS073670NINDS NIH HHS R01 NS073670
6 · The paper itself

Abstract

Inflammation is closely intertwined with pathogenesis of Parkinson's disease (PD). Increasing evidence suggests that inhibition of glia-mediated inflammation might represent a promising therapeutic target for PD. Glia maturation factor (GMF), an inflammatory protein, predominantly localized in astrocytes is previously isolated, sequenced and cloned in our laboratory. In the present investigation, we demonstrate that GMF-deficiency in astrocytes upregulates the antioxidant status and limit the extent of lipid peroxidation and production of reactive oxygen species (ROS) along with diminished nuclear factor-κB-mediated inflammatory responses in 1-methyl-4-phenylpyridinium (MPP(+))-induced toxicity. Primary astrocytes obtained from wild-type (Wt) and GMF-deficient (GMF-KO) mice were treated with 5, 10, and 20 μM MPP(+) for 24, 48, and 72 h in vitro. Our results show decreased release of ROS and increased level of glutathione in astrocytes obtained from GMF-KO mice when compared to astrocytes derived from Wt mice following MPP(+) treatment. Additionally, we found decreased activity of NF-κB, and reduced levels of proinflammatory tumor necrosis factor- α, interleukin-1β (IL-1β), IL-17, IL-33, and chemokine (C-C motif) ligand 2 (CCL2) in GMF-KO astrocytes when compared to Wt astrocytes. Our overall results suggest that GMF-KO astrocytes are significantly resistant to MPP(+) toxicity when compared to Wt astrocytes.

Indexed as

Oxidative Stress1-Methyl-4-phenylpyridiniumAnimalsAstrocytesCells, CulturedChemokine CCL2Glia Maturation FactorInterleukinsLipid PeroxidationMiceMice, Inbred C57BLNF-kappa BReactive Oxygen SpeciesTumor Necrosis Factor-alpha1-Methyl-4-phenylpyridiniumCcl2 protein, mouseChemokine CCL2Glia Maturation FactorInterleukinsNF-kappa BReactive Oxygen SpeciesTumor Necrosis Factor-alpha

Identifiers

PMID24430624
PMCPMC4101074
OpenAlexW1991906033

What OpenQuestion holds

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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.