Evidence map›Paper›PMID 12736340›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003

Heme oxygenase-2 protects against lipid peroxidation-mediated cell loss and impaired motor recovery after traumatic brain injury.

Edward F Chang, Ronald J Wong, Hendrik J Vreman, Takuji Igarashi, Ethel Galo, Frank R Sharp, David K Stevenson, Linda J Noble-Haeusslein

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

65 citing papers in PubMed, 120 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. DNA Double-Strand Breaks as Pathogenic Lesions in Neurological Disorders.International journal of molecular sciences · 2022
    Review
  11. Article
  12. Carbon Monoxide: from Poison to Clinical Trials.Trends in pharmacological sciences · 2021
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

5 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

8 authors at 3 institutions in 1 country.

Edward F ChangDepartment of Neurosurgery, University of California, San Francisco, San Francisco, California 94143-0520, USA.
Ronald J Wong
Hendrik J Vreman
Takuji Igarashi
Ethel Galo
Frank R Sharp
David K Stevenson
Linda J Noble-Haeusslein
University of California, San Francisco · USStanford University · USUniversity of Cincinnati · US

Funding

Trauma to Developing Brain-Oxidative Events and RecoveryR21NS041256 · NINDS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI NOBLE, LINDA J. · 2002 to 2004
$544k
NINDS NIH HHS NS 41256NINDS NIH HHS R21 NS041256
6 · The paper itself

Abstract

After traumatic brain injury (TBI), substantial extracellular heme is released from hemoproteins during hemorrhage and cell injury. Heme oxygenase (HO) isozymes are thought to detoxify the pro-oxidant heme to the potent antioxidant, bilirubin. HO-1, the inducible isozyme, is expressed in glial populations after injury and may play a protective role. However, the role of HO-2, the predominant and constitutively expressed isozyme in the brain, remains unclear after TBI. We used a controlled cortical impact injury model to determine the extent and mechanism of damage between HO-2 knock-out (KO) (-/-) and wild-type (WT) (+/+) mice. The specific cellular and temporal expressions of HO-2 and HO-1 were characterized by immunocytochemistry and Western blots. HO-2 was immunolocalized in neurons both before and after TBI, whereas HO-1 was highly upregulated in glia only after TBI. HO activity determined by gas chromatography using brain sonicates from injured HO-2 KO mice was significantly less than that of HO-2 wild types, despite the induction of HO-1 expression after TBI. Cell loss was significantly greater in KO mice in areas including the cortex, the CA3 region of hippocampus, and the lateral dorsal thalamus. Furthermore, motor recovery after injury, as measured by the rotarod assay and an inclined beam-walking task, was compromised in the KO mice. Finally, brain tissue from injured HO-2 KO mice exhibited decreased ability to reduce oxidative stress, as measured with an Fe(2+)/ascorbic acid-mediated carbon monoxide generation assay for lipid peroxidation susceptibility. These findings demonstrate that HO-2 expression protects neurons against TBI by reducing lipid peroxidation via the catabolism of free heme.

Indexed as

Lipid PeroxidationRecovery of FunctionAnimalsBehavior, AnimalBrainBrain InjuriesCell CountDisease Models, AnimalEnzyme ActivationEnzyme InductionHemeHeme Oxygenase-1Heme Oxygenase (Decyclizing)ImmunohistochemistryIsoenzymesMaleHemeHeme Oxygenase-1heme oxygenase-2Heme Oxygenase (Decyclizing)Hmox1 protein, mouseIsoenzymesMembrane Proteins

Identifiers

PMID12736340
PMCPMC6742170
OpenAlexW2111967645

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.