Evidence map›Paper›PMID 26219598›Full record

ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2015

Knockout of silent information regulator 2 (SIRT2) preserves neurological function after experimental stroke in mice.

Lea Krey, Fred Lühder, Kathrin Kusch, Bozena Czech-Zechmeister, Birte Könnecke, Tiago Fleming Outeiro, George Trendelenburg

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. Review
  3. mMolecular neurobiology · 2024
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  6. Role of NADCellular and molecular neurobiology · 2023
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  7. Review
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  10. Review
  11. Article
  12. Review
  13. Article
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  15. Article
  16. Article
  17. The NADAntioxidants & redox signaling · 2018
    Review
  18. Article
  19. Article
  20. Could Sirtuin Activities Modify ALS Onset and Progression?Cellular and molecular neurobiology · 2017
    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

7 authors at 2 institutions in 1 country.

Lea KreyDepartment of Neurology, University Medical Center Göttingen, Göttingen, Germany.
Fred LühderDepartment of Neuroimmunology, Institute for Multiple Sclerosis Research, University Medical Center Göttingen, Göttingen, Germany.
Kathrin KuschDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, Göttingen, Germany.
Bozena Czech-ZechmeisterDepartment of Neurology, University Medical Center Göttingen, Göttingen, Germany.
Birte KönneckeDepartment of Neurology, University Medical Center Göttingen, Göttingen, Germany.
Tiago Fleming OuteiroCenter for Nanoscale Microscopy and Molecular Physiology of the Brain, Department of Neurodegeneration and Restorative Research, University Medical Center Göttingen, Göttingen, Germany.
George TrendelenburgDepartment of Neurology, University Medical Center Göttingen, Göttingen, Germany.
Universitätsmedizin Göttingen · DEMax Planck Institute of Experimental Medicine · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sirtuin-2 (Sirt2) is a member of the NAD(+)-dependent protein deacetylase family. Various members of the sirtuin class have been found to be involved in processes related to longevity, regulation of inflammation, and neuroprotection. Induction of Sirt2 mRNA was found in the whole hemisphere after experimental stroke in a recent screening approach. Moreover, Sirt2 protein is highly expressed in myelin-rich brain regions after stroke. To examine the effects of Sirt2 on ischemic stroke, we induced transient focal cerebral ischemia in adult male Sirt2-knockout and wild-type mice. Two stroke models with different occlusion times were applied: a severe ischemia (45 minutes of middle cerebral artery occlusion (MCAO)) and a mild one (15 minutes of MCAO), which was used to focus on subcortical infarcts. Neurological deficit was determined at 48 hours after 45 minutes of MCAO, and up to 7 days after induction of 15 minutes of cerebral ischemia. In contrast to recent data on Sirt1, Sirt2(-/-) mice showed less neurological deficits in both models of experimental stroke, with the strongest manifestation after 48 hours of reperfusion. However, we did not observe a significant difference of stroke volumes or inflammatory cell count between Sirt2-deficient and wild-type mice. Thus we postulate that Sirt2 mediates myelin-dependent neuronal dysfunction during the early phase after ischemic stroke.

Indexed as

AnimalsBrainBrain IschemiaCell CountGene ExpressionInfarction, Middle Cerebral ArteryInflammationIschemic Attack, TransientMiceMice, Inbred C57BLMice, KnockoutNervous System DiseasesReperfusion InjuryRNA, MessengerSirtuin 2SirtuinsRNA, MessengerSirt2 protein, mouseSirtuin 2Sirtuins

Identifiers

PMID26219598
PMCPMC4671131
OpenAlexW1949548600

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.