Evidence map›Paper›PMID 27126323›Full record

ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2017

Lithium-induced neuroprotection in stroke involves increased miR-124 expression, reduced RE1-silencing transcription factor abundance and decreased protein deubiquitination by GSK3β inhibition-independent pathways.

Thorsten R Doeppner, Britta Kaltwasser, Eduardo H Sanchez-Mendoza, Ahmet B Caglayan, Mathias Bähr, Dirk M Hermann

Erratum issuedOpen access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

25 citing papers in PubMed, 43 citations in OpenAlex.

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  9. Rbfox-1 contributes to CaMKIIα expression and intracerebral hemorrhage-induced secondary brain injury via blocking micro-RNA-124.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
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  18. The Potential Role of MicroRNA-124 in Cerebral Ischemia Injury.International journal of molecular sciences · 2019
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Thorsten R Doeppner1 Department of Neurology, University of Duisburg-Essen, Essen, Germany.
Britta Kaltwasser1 Department of Neurology, University of Duisburg-Essen, Essen, Germany.
Eduardo H Sanchez-Mendoza1 Department of Neurology, University of Duisburg-Essen, Essen, Germany.
Ahmet B Caglayan2 Regenerative and Restorative Medical Research Center, Istanbul Medipol University, Istanbul, Turkey.
Mathias Bähr3 Department of Neurology, University of Göttingen Medical School, Göttingen, Germany.
Dirk M Hermann1 Department of Neurology, University of Duisburg-Essen, Essen, Germany.
University of Duisburg-Essen · DEIstanbul Medipol University · TRUniversity of Göttingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lithium promotes acute poststroke neuronal survival, which includes mechanisms that are not limited to GSK3β inhibition. However, whether lithium induces long-term neuroprotection and enhanced brain remodeling is unclear. Therefore, mice were exposed to transient middle cerebral artery occlusion and lithium (1 mg/kg bolus followed by 2 mg/kg/day over up to 7 days) was intraperitoneally administered starting 0-9 h after reperfusion onset. Delivery of lithium no later than 6 h reduced infarct volume on day 2 and decreased brain edema, leukocyte infiltration, and microglial activation, as shown by histochemistry and flow cytometry. Lithium-induced neuroprotection persisted throughout the observation period of 56 days and was associated with enhanced neurological recovery. Poststroke angioneurogenesis and axonal plasticity were also enhanced by lithium. On the molecular level, lithium increased miR-124 expression, reduced RE1-silencing transcription factor abundance, and decreased protein deubiquitination in cultivated cortical neurons exposed to oxygen-glucose deprivation and in brains of mice exposed to cerebral ischemia. Notably, this effect was not mimicked by pharmacological GSK3β inhibition. This study for the first time provides efficacy data for lithium in the postacute ischemic phase, reporting a novel mechanism of action, i.e. increased miR-124 expression facilitating REST degradation by which lithium promotes postischemic neuroplasticity and angiogenesis.

Indexed as

AnimalsGlycogen Synthase Kinase 3 betaInfarction, Middle Cerebral ArteryLithiumMiceMicroRNAsNeovascularization, PhysiologicNeuronal PlasticityNeuroprotectionRE1-Silencing Transcription FactorRepressor ProteinsStrokeUbiquitinationGlycogen Synthase Kinase 3 betaLithiumMicroRNAsMirn124 microRNA, mouseRE1-Silencing Transcription FactorRepressor ProteinsCerebral ischemialithiummiRNAneuroregenerationRE1-silencing transcription factorstroke

Identifiers

PMID27126323
PMCPMC5363471
OpenAlexW2342919482

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.