Evidence map›Paper›PMID 19179380›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2009

Activation of Ets-2 by oxidative stress induces Bcl-xL expression and accounts for glial survival in amyotrophic lateral sclerosis.

Junghee Lee, Mari Kannagi, Robert J Ferrante, Neil W Kowall, Hoon Ryu

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2009. 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
2.1field-weighted citation impact, top 12% 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, 40 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Nutritional Regulators of Bcl-xL in the Brain.Molecules (Basel, Switzerland) · 2018
    Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
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

5 authors at 4 institutions in 2 countries.

Junghee LeeDepartment of Neurology, Boston University School of Medicine, Boston, Massachusetts, USA. junghee@bu.edu
Mari Kannagi
Robert J Ferrante
Neil W Kowall
Hoon Ryu
VA Boston Healthcare System · USBedford VA Research Corporation · USBoston University · USTokyo Medical and Dental University · JP

Funding

Neuropathology CoreP30AG013846 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI KOWALL, NEIL W. · 1996 to 2020
$29.1M
Transcription and Therapy for HD: from Molecules to ManP01NS045242 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI KRAINC, DIMITRI · 2003 to 2007
$6.3M
Combination Drug Therapy in Huntington's DiseaseU01NS045806 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI FERRANTE, ROBERT J · 2004 to 2008
$3.0M
Estrogen Regulation of Mitochondrial Transcription in HDR01NS052724 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI RYU, HOON · 2005 to 2009
$1.3M
NIA NIH HHS P30 AG013846NIA NIH HHS P30 AG-13846NINDS NIH HHS NS045242NINDS NIH HHS NS045806NINDS NIH HHS NS-52724NINDS NIH HHS P01 NS045242NINDS NIH HHS R01 NS052724NINDS NIH HHS U01 NS045806
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is an adult-onset neurodegenerative disease characterized by selective degeneration of motor neurons and glial activation. Cell-specific transcriptional regulation induced by oxidative stress may contribute to the survival and activation of astrocytes in the face of motor neuron death. In the present study, we demonstrate an age-dependent increase in Bcl-xL and Ets-2 immunoreactivity that correlates with an increase of glial fibrillary acidic protein (GFAP)-positive cells in the ventral horn of the spinal cord in both ALS transgenic mice [mutant SOD1 (G93A)] and affected humans. Chromatin immunoprecipitation (ChIP) analysis verified that Ets-2 preferentially occupies the Ets-2 binding element in the promoter of Bcl-xL in primary astrocytes under oxidative stress conditions as well as in G93A spinal cords. Ets-2 small-interfering RNA down-regulated the transcriptional activity of Bcl-xL. In primary glial cultures, Bcl-xL overexpression and mutant SOD1 (G93A) both conferred resistance to oxidative stress-induced cell death. Our findings suggest that Ets-2 transcription factor activation of Bcl-xL gene may protect glia from constitutive oxidative stress that is thought to be a key mechanism contributing to the pathogenesis of ALS. This survival pathway may contribute to the glial survival and activation seen in the spinal cord of ALS patients.

Indexed as

Amyotrophic Lateral SclerosisAnimalsbcl-X ProteinCells, CulturedCell SurvivalDisease Models, AnimalFemaleGlial Fibrillary Acidic ProteinHumansMaleMiceMice, TransgenicMotor NeuronsNeurogliaNF-kappa BOxidative Stressbcl-X ProteinGlial Fibrillary Acidic ProteinNF-kappa BProto-Oncogene Protein c-ets-2SOD1 G93A proteinSp1 Transcription FactorSuperoxide Dismutase

Identifiers

PMID19179380
PMCPMC2698657
OpenAlexW2121729487

What OpenQuestion holds

Textmetadata
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.