Evidence map›Paper›PMID 23350672›Full record

ArticleJournal of neurochemistry2013

Mechanisms of neuroprotection by hemopexin: modeling the control of heme and iron homeostasis in brain neurons in inflammatory states.

Peter Hahl, Taron Davis, Cecilia Washburn, Jack T Rogers, Ann Smith

Open access · greenAbstract read
In one paragraph

Article in Journal of neurochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

42 citing papers in PubMed, 80 citations in OpenAlex.

  1. Article
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  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. New Insights into Hemopexin-Binding to Hemin and Hemoglobin.International journal of molecular sciences · 2022
    Article
  12. Heme Oxygenase 1 in Vertebrates: Friend and Foe.Cell biochemistry and biophysics · 2022
    Review
  13. Review
  14. Review
  15. Human Plasma and Recombinant Hemopexins: Heme Binding Revisited.International journal of molecular sciences · 2021
    Article
  16. Review
  17. Review
  18. Article
  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 3 institutions in 1 country.

Peter HahlSchool of Biological Sciences, University of Missouri - Kansas City, Kansas City, MO, USA.
Taron Davis
Cecilia Washburn
Jack T Rogers
Ann Smith
University of Missouri–Kansas City · USHarvard University · USMassachusetts General Hospital · US

Funding

Post Transcriptional Control of hemorrhagic iron damage.R21NS077079 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI ROGERS, JACK T · 2012 to 2013
$458k
Mechanisms of Heme TransportR21DK064363 · NIDDK · UNIVERSITY OF MISSOURI KANSAS CITY · PI SMITH, ANN · 2004 to 2005
$294k
NIDDK NIH HHS R21 DK064363NIDDK NIH HHS R21DK64363NINDS NIH HHS R21 NS077079
6 · The paper itself

Abstract

Hemopexin provides neuroprotection in mouse models of stroke and intracerebral hemorrhage and protects neurons in vitro against heme or reactive oxygen species (ROS) toxicity via heme oxygenase-1 (HO1) activity. To model human brain neurons experiencing hemorrhages and inflammation, we used human neuroblastoma cells, heme-hemopexin complexes, and physiologically relevant ROS, for example, H(2)O(2) and HOCl, to provide novel insights into the underlying mechanism whereby hemopexin safely maintains heme and iron homeostasis. Human amyloid precursor protein (hAPP), needed for iron export from neurons, is induced ~twofold after heme-hemopexin endocytosis by iron from heme catabolism via the iron-regulatory element of hAPP mRNA. Heme-hemopexin is relatively resistant to damage by ROS and retains its ability to induce the cytoprotective HO1 after exposure to tert-butylhydroperoxide, although induction is impaired, but not eliminated, by exposure to high concentrations of H(2)O(2) in vitro. Apo-hemopexin, which predominates in non-hemolytic states, resists damage by H(2)O(2) and HOCl, except for the highest concentrations likely in vivo. Heme-albumin and albumin are preferential targets for ROS; thus, albumin protects hemopexin in biological fluids like CSF and plasma where it is abundant. These observations provide strong evidence that hemopexin will be neuroprotective after traumatic brain injury, with heme release in the CNS, and during the ensuing inflammation. Hemopexin sequesters heme, thus preventing unregulated heme uptake that leads to toxicity; it safely delivers heme to neuronal cells; and it activates the induction of proteins including HO1 and hAPP that keep heme and iron at safe levels in neurons.

Indexed as

Amyloid beta-Protein PrecursorApoproteinsBrainBrain InjuriesCell Line, TumorCerebral HemorrhageEndocytosisEnzyme InductionHemeHeme Oxygenase-1HemopexinHumansInflammationNeuronsPeroxidesReactive Oxygen SpeciesAmyloid beta-Protein PrecursorApoproteinsHemeHeme Oxygenase-1HemopexinPeroxidesReactive Oxygen Species

Identifiers

PMID23350672
PMCPMC3752430
OpenAlexW1987505659

What OpenQuestion holds

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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.