Evidence map›Paper›PMID 26928051›Full record

ArticleASN neuro

Astrocytic Ephrin-B1 Regulates Synapse Remodeling Following Traumatic Brain Injury.

Angeliki M Nikolakopoulou, Jordan Koeppen, Michael Garcia, Joshua Leish, Andre Obenaus, Iryna M Ethell

Open access · goldAbstract read
In one paragraph

Article in ASN neuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

32 citing papers in PubMed, 72 citations in OpenAlex.

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  4. MNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
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  20. The synapse in traumatic brain injury.Brain : a journal of neurology · 2021
    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

6 authors at 2 institutions in 1 country.

Angeliki M NikolakopoulouBiomedical Sciences Division, School of Medicine, University of California Riverside, CA, USA.
Jordan KoeppenBiomedical Sciences Division, School of Medicine, University of California Riverside, CA, USA Cell, Molecular, and Developmental Biology graduate program, University of California Riverside, CA, USA.
Michael GarciaBiomedical Sciences Division, School of Medicine, University of California Riverside, CA, USA.
Joshua LeishBiomedical Sciences Division, School of Medicine, University of California Riverside, CA, USA.
Andre ObenausDepartment of Pediatrics, School of Medicine, Loma Linda University, CA, USA.
Iryna M EthellBiomedical Sciences Division, School of Medicine, University of California Riverside, CA, USA Cell, Molecular, and Developmental Biology graduate program, University of California Riverside, CA, USA iryna.ethell@ucr.edu.
University of California, Riverside · USLoma Linda University · US

Funding

EphB Signaling in Dendritic Spine Development and RemodelingR01MH067121 · NIMH · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI ETHELL, IRYNA M · 2003 to 2017
$4.6M
NIMH NIH HHS MH67121NIMH NIH HHS R01 MH067121
6 · The paper itself

Abstract

Traumatic brain injury (TBI) can result in tissue alterations distant from the site of the initial injury, which can trigger pathological changes within hippocampal circuits and are thought to contribute to long-term cognitive and neuropsychological impairments. However, our understanding of secondary injury mechanisms is limited. Astrocytes play an important role in brain repair after injury and astrocyte-mediated mechanisms that are implicated in synapse development are likely important in injury-induced synapse remodeling. Our studies suggest a new role of ephrin-B1, which is known to regulate synapse development in neurons, in astrocyte-mediated synapse remodeling following TBI. Indeed, we observed a transient upregulation of ephrin-B1 immunoreactivity in hippocampal astrocytes following moderate controlled cortical impact model of TBI. The upregulation of ephrin-B1 levels in hippocampal astrocytes coincided with a decline in the number of vGlut1-positive glutamatergic input to CA1 neurons at 3 days post injury even in the absence of hippocampal neuron loss. In contrast, tamoxifen-induced ablation of ephrin-B1 from adult astrocytes in ephrin-B1(loxP/y)ERT2-Cre(GFAP) mice accelerated the recovery of vGlut1-positive glutamatergic input to CA1 neurons after TBI. Finally, our studies suggest that astrocytic ephrin-B1 may play an active role in injury-induced synapse remodeling through the activation of STAT3-mediated signaling in astrocytes. TBI-induced upregulation of STAT3 phosphorylation within the hippocampus was suppressed by astrocyte-specific ablation of ephrin-B1 in vivo, whereas the activation of ephrin-B1 in astrocytes triggered an increase in STAT3 phosphorylation in vitro. Thus, regulation of ephrin-B1 signaling in astrocytes may provide new therapeutic opportunities to aid functional recovery after TBI.

Indexed as

AnimalsAstrocytesBrain Injuries, TraumaticCA1 Region, HippocampalCells, CulturedDisease Models, AnimalEphrin-B1GliosisMaleMice, Inbred C57BLMice, TransgenicPhosphorylationSTAT3 Transcription FactorSynapsesVesicular Glutamate Transport Protein 1Efnb1 protein, mouseEphrin-B1Slc17a7 protein, mouseStat3 protein, mouseSTAT3 Transcription FactorVesicular Glutamate Transport Protein 1astrocytesephrinB1hippocampusSTAT3synapsetraumatic brain injury

Identifiers

PMID26928051
PMCPMC4774052
OpenAlexW2292924020

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.