Evidence map›Paper›PMID 26715414›Full record

ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2016

Beneficial Effect of Erythropoietin Short Peptide on Acute Traumatic Brain Injury.

Bo Wang, Mitchell Kang, Michelle Marchese, Esther Rodriguez, Wei Lu, Xintong Li, Yasuhiro Maeda, Peter Dowling

Open access · bronzeAbstract read
In one paragraph

Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 21% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Does erythropoietin affect the outcome and complication rates of patient with traumatic brain injury? A pooled-analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022
    Pooled it
  2. Review
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  6. Article
  7. Frontiers in aging neuroscience · 2019
    Article
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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 2 institutions in 1 country.

Bo WangNeurology Service, VA Medical Center of East Orange, East Orange, NJ, USA.
Mitchell KangNeurology Service, VA Medical Center of East Orange, East Orange, NJ, USA.
Michelle MarcheseNeurology Service, VA Medical Center of East Orange, East Orange, NJ, USA.
Esther RodriguezNeurology Service, VA Medical Center of East Orange, East Orange, NJ, USA.
Wei LuNeurology Service, VA Medical Center of East Orange, East Orange, NJ, USA.
Xintong LiNeurology Service, VA Medical Center of East Orange, East Orange, NJ, USA.
Yasuhiro MaedaNeurology Service, VA Medical Center of East Orange, East Orange, NJ, USA.
Peter DowlingNeurology Service, VA Medical Center of East Orange, East Orange, NJ, USA. dowlinpc@njms.rutgers.edu.
East Orange VA Medical Center · USRutgers New Jersey Medical School

Funding

New generation EPO peptides with enhanced safety for acute TBII01RX000220 · VA · VA NEW JERSEY HEALTH CARE SYSTEM · PI DOWLING, PETER C · 2009 to 2015
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Novel EPO peptide therapy for a new mouse model of dementiaI01RX001305 · VA · VA NEW JERSEY HEALTH CARE SYSTEM · PI DOWLING, PETER C · 2015 to 2019
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RRD VA I01 RX000220RRD VA I01 RX001305
6 · The paper itself

Abstract

There is currently no effective medical treatment for traumatic brain injury (TBI). Beyond the immediate physical damage caused by the initial impact, additional damage evolves due to the inflammatory response that follows brain injury. Here we show that therapy with JM4, a low molecular weight 19-amino acid nonhematopoietic erythropoietin (EPO) peptidyl fragment, containing amino acids 28-46 derived from the first loop of EPO, markedly reduces acute brain injury. Mice underwent controlled cortical injury and received either whole molecule EPO, JM4, or sham-treatment with phosphate-buffered saline. Animals treated with JM4 peptide exhibited a large decrease in number of dead neural cells and a marked reduction in lesion size at both 3 and 8 days postinjury. Therapy with JM4 also led to improved functional recovery and we observed a treatment window for JM4 peptide that remained open for at least 9 h postinjury. The full-length EPO molecule was divided into a series of 6 contiguous peptide segments; the JM4-containing segment and the adjoining downstream region contained the bulk of the death attenuating effects seen with intact EPO molecule following TBI. These findings indicate that the JM4 molecule substantially blocks cell death and brain injury following acute brain trauma and, as such, presents an excellent opportunity to explore the therapeutic potential of a small-peptide EPO derivative in the medical treatment of TBI.

Indexed as

AnimalsBlood-Brain BarrierBrainBrain Injuries, TraumaticCell DeathErythropoietinIn Situ Nick-End LabelingMaleMiceMice, Inbred C57BLNeuroprotective AgentsPeptide FragmentsErythropoietinerythropoietin (28-46)Neuroprotective AgentsPeptide FragmentsErythropoietinNeuroprotectionSmall peptide therapyTraumatic brain injury

Identifiers

PMID26715414
PMCPMC4824022
OpenAlexW2199546945

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.