Evidence map›Paper›PMID 29383690›Full record

ArticleMolecular neurobiology2018

Glia Maturation Factor Dependent Inhibition of Mitochondrial PGC-1α Triggers Oxidative Stress-Mediated Apoptosis in N27 Rat Dopaminergic Neuronal Cells.

Govindhasamy Pushpavathi Selvakumar, Shankar S Iyer, Duraisamy Kempuraj, Murugesan Raju, Ramasamy Thangavel, Daniyal Saeed, Mohammad Ejaz Ahmed, Harris Zahoor, Sudhanshu P Raikwar, Smita Zaheer and 1 more

Abstract read
In one paragraph

Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

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  16. Frontiers in neuroscience · 2020
    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. 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
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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

11 authors at 2 institutions in 1 country.

Govindhasamy Pushpavathi SelvakumarHarry S. Truman Memorial Veterans Hospital, Columbia, MO, USA.
Shankar S IyerHarry S. Truman Memorial Veterans Hospital, Columbia, MO, USA.
Duraisamy KempurajHarry S. Truman Memorial Veterans Hospital, Columbia, MO, USA.
Murugesan RajuDepartment of Ophthalmology, University of Missouri, Columbia, MO, USA.
Ramasamy ThangavelHarry S. Truman Memorial Veterans Hospital, Columbia, MO, USA.
Daniyal SaeedDepartment of Neurology and The Center for Translational Neuroscience, M741A Medical Science Building, School of Medicine, University of Missouri, 1 Hospital Drive, Columbia, MO, USA.
Mohammad Ejaz AhmedDepartment of Neurology and The Center for Translational Neuroscience, M741A Medical Science Building, School of Medicine, University of Missouri, 1 Hospital Drive, Columbia, MO, USA.
Harris ZahoorDepartment of Neurology and The Center for Translational Neuroscience, M741A Medical Science Building, School of Medicine, University of Missouri, 1 Hospital Drive, Columbia, MO, USA.
Sudhanshu P RaikwarHarry S. Truman Memorial Veterans Hospital, Columbia, MO, USA.
Smita ZaheerDepartment of Neurology and The Center for Translational Neuroscience, M741A Medical Science Building, School of Medicine, University of Missouri, 1 Hospital Drive, Columbia, MO, USA.
Asgar ZaheerHarry S. Truman Memorial Veterans Hospital, Columbia, MO, USA. zaheera@health.missouri.edu.ORCID http://orcid.org/0000-0003-3344-0371
University of Missouri Hospital · USUniversity of Missouri · 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 BX002477Foundation for the National Institutes of Health NS073670NIA NIH HHS AG048205NIA NIH HHS R01 AG048205NINDS NIH HHS R01 NS073670U.S. Department of Veterans Affairs I01BX002477
6 · The paper itself

Abstract

Parkinson's disease (PD) is a progressive neurodegenerative disease affecting over five million individuals worldwide. The exact molecular events underlying PD pathogenesis are still not clearly known. Glia maturation factor (GMF), a neuroinflammatory protein in the brain plays an important role in the pathogenesis of PD. Mitochondrial dysfunctions and oxidative stress trigger apoptosis leading to dopaminergic neuronal degeneration in PD. Peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC-1α or PPARGC-α) acts as a transcriptional co-regulator of mitochondrial biogenesis and energy metabolism by controlling oxidative phosphorylation, antioxidant activity, and autophagy. In this study, we found that incubation of immortalized rat dopaminergic (N27) neurons with GMF influences the expression of peroxisome PGC-1α and increases oxidative stress, mitochondrial dysfunction, and apoptotic cell death. We show that incubation with GMF reduces the expression of PGC-1α with concomitant decreases in the mitochondrial complexes. Besides, there is increased oxidative stress and depolarization of mitochondrial membrane potential (MMP) in these cells. Further, GMF reduces tyrosine hydroxylase (TH) expression and shifts Bax/Bcl-2 expression resulting in release of cytochrome-c and increased activations of effector caspase expressions. Transmission electron microscopy analyses revealed alteration in the mitochondrial architecture. Our results show that GMF acts as an important upstream regulator of PGC-1α in promoting dopaminergic neuronal death through its effect on oxidative stress-mediated apoptosis. Our current data suggest that GMF is a critical risk factor for PD and suggest that it could be explored as a potential therapeutic target to inhibit PD progression.

Indexed as

Adenosine TriphosphateAnimalsApoptosisbcl-2-Associated X ProteinCaspasesCell LineCell ProliferationCell SurvivalChromatinCytochromes cCytosolDopaminergic NeuronsEnzyme ActivationGlia Maturation FactorHumansMembrane Potential, MitochondrialAdenosine Triphosphatebcl-2-Associated X ProteinCaspasesChromatinCytochromes cGlia Maturation FactorPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, ratReactive Oxygen SpeciesTyrosine 3-MonooxygenaseApoptosisDysfunctionsMitochondrialNeurodegenerationOxidative stressParkinson’s disease

Identifiers

PMID29383690
PMCPMC6066475
OpenAlexW2792230854

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.