Evidence map›Paper›PMID 20224768›Full record

ArticlePloS one2010

Disruption of astrocyte STAT3 signaling decreases mitochondrial function and increases oxidative stress in vitro.

Theodore A Sarafian, Cindy Montes, Tetsuya Imura, Jingwei Qi, Giovanni Coppola, Daniel H Geschwind, Michael V Sofroniew

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

103 citing papers in PubMed, 150 citations in OpenAlex.

  1. Review
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  8. Article
  9. Article
  10. Article
  11. Review
  12. The JAK-STAT Signaling Pathway in Epilepsy.Current neuropharmacology · 2023
    Review
  13. Article
  14. Article
  15. Review
  16. The role of astrocytes in neuropathic pain.Frontiers in molecular neuroscience · 2022
    Review
  17. Article
  18. Review
  19. IL-6 enhances CD4 cell motility by sustaining mitochondrial CaProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  20. Review

43 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

7 authors at 1 institution in 1 country.

Theodore A SarafianDepartment of Neurobiology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, United States of America. tsarafian@mednet.ucla.edu
Cindy Montes
Tetsuya Imura
Jingwei Qi
Giovanni Coppola
Daniel H Geschwind
Michael V Sofroniew
University of California, Los Angeles · US

Funding

Molecular Dissection of Reactive Astrogliosis: STAT3R01NS057624 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SOFRONIEW, MICHAEL V · 2008 to 2012
$1.8M
Pulmonary Mitochondrial Injury Caused by TetrahydrocannabinolR21DA021580 · NIDA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SARAFIAN, THEODORE A · 2006 to 2007
$305k
NIDA NIH HHS DA021580NIDA NIH HHS R21 DA021580NINDS NIH HHS 5R01NS057624NINDS NIH HHS R01 NS057624
6 · The paper itself

Abstract

backgroundAstrocytes exert a wide variety of functions in health and disease and respond to a wide range of signaling pathways, including members of the Janus-kinase signal transducers and activators of transcription (Jak-STAT) family. We have recently shown that STAT3 is an important regulator of astrocyte reactivity after spinal cord injury in vivo[1]. METHODOLOGY/PRINCIPAL

findingsHere, we used both a conditional gene deletion strategy that targets the deletion of STAT3 selectively to astrocytes (STAT3-CKO), and a pharmacological inhibitor of JAK-2, AG490, in cultured astrocytes in vitro, to investigate potential functions and molecules influenced by STAT3 signaling in relation to mitochondrial function and oxidative stress. Our findings show that the absence of STAT3 signaling in astrocytes leads to (i) increased production of superoxide anion and other reactive oxygen species and decreased level of glutathione, (ii) decreased mitochondrial membrane potential and decreased ATP production, and (iii) decreased rate of cell proliferation. Many of the differences observed in STAT3-CKO astrocytes were distinctly altered by exposure to rotenone, suggesting a role for complex I of the mitochondrial electron transport chain. Gene expression microarray studies identified numerous changes in STAT3-CKO cells that may have contributed to the identified deficits in cell function. CONCLUSIONS/SIGNIFICANCE: Taken together, these STAT3-dependent alterations in cell function and gene expression have relevance to both reactive gliosis and to the support and protection of surrounding cells in neural tissue.

Indexed as

Oxidative StressAdenosine TriphosphateAnimalsAntioxidantsAstrocytesCell ProliferationGene DeletionGenotypeGlutathioneImmunohistochemistryMembrane PotentialsMiceMitochondriaSignal TransductionSTAT3 Transcription FactorAdenosine TriphosphateAntioxidantsGlutathioneSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID20224768
PMCPMC2835741
OpenAlexW2054737835

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.