Evidence map›Paper›PMID 26673668›Full record

ArticleCell death & disease2015

Cellular prion protein promotes post-ischemic neuronal survival, angioneurogenesis and enhances neural progenitor cell homing via proteasome inhibition.

T R Doeppner, B Kaltwasser, J Schlechter, J Jaschke, E Kilic, M Bähr, D M Hermann, J Weise

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

28 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Prospects and challenges of tissue-derived extracellular vesicles.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. The multiple functions of PrPJournal of molecular medicine (Berlin, Germany) · 2022
    Review
  8. Article
  9. Evidence for the Benefits of Melatonin in Cardiovascular Disease.Frontiers in cardiovascular medicine · 2022
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article
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 5 institutions in 2 countries.

T R DoeppnerDepartment of Neurology, University of Duisburg-Essen Medical School, Essen, Germany.
B KaltwasserDepartment of Neurology, University of Duisburg-Essen Medical School, Essen, Germany.
J SchlechterDepartment of Neurology, University of Duisburg-Essen Medical School, Essen, Germany.
J JaschkeDepartment of Neurology, University of Jena, Jena, Germany.
E KilicRegenerative and Restorative Medical Research Center, Istanbul Medipol University, Istanbul, Turkey.
M BährDepartment of Neurology, University of Goettingen, Goettingen, Germany.
D M HermannDepartment of Neurology, University of Duisburg-Essen Medical School, Essen, Germany.
J WeiseDepartment of Neurology, University of Jena, Jena, Germany.
University of Duisburg-Essen · DEIstanbul Medipol University · TRFriedrich Schiller University Jena · DEHelios Vogtland Klinikum Plauen · DEUniversity of Göttingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although cellular prion protein (PrP(c)) has been suggested to have physiological roles in neurogenesis and angiogenesis, the pathophysiological relevance of both processes remain unknown. To elucidate the role of PrP(c) in post-ischemic brain remodeling, we herein exposed PrP(c) wild type (WT), PrP(c) knockout (PrP-/-) and PrP(c) overexpressing (PrP+/+) mice to focal cerebral ischemia followed by up to 28 days reperfusion. Improved neurological recovery and sustained neuroprotection lasting over the observation period of 4 weeks were observed in ischemic PrP+/+ mice compared with WT mice. This observation was associated with increased neurogenesis and angiogenesis, whereas increased neurological deficits and brain injury were noted in ischemic PrP-/- mice. Proteasome activity and oxidative stress were increased in ischemic brain tissue of PrP-/- mice. Pharmacological proteasome inhibition reversed the exacerbation of brain injury induced by PrP-/-, indicating that proteasome inhibition mediates the neuroprotective effects of PrP(c). Notably, reduced proteasome activity and oxidative stress in ischemic brain tissue of PrP+/+ mice were associated with an increased abundance of hypoxia-inducible factor 1α and PACAP-38, which are known stimulants of neural progenitor cell (NPC) migration and trafficking. To elucidate effects of PrP(c) on intracerebral NPC homing, we intravenously infused GFP(+) NPCs in ischemic WT, PrP-/- and PrP+/+ mice, showing that brain accumulation of GFP(+) NPCs was greatly reduced in PrP-/- mice, but increased in PrP+/+ animals. Our results suggest that PrP(c) induces post-ischemic long-term neuroprotection, neurogenesis and angiogenesis in the ischemic brain by inhibiting proteasome activity.

Indexed as

AnimalsBrain IschemiaDisease Models, AnimalMaleMiceMice, TransgenicNeural Stem CellsNeurogenesisNeuronsNeuroprotective AgentsPrionsNeuroprotective AgentsPrions

Identifiers

PMID26673668
PMCPMC4720898
OpenAlexW2208280417

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.