Evidence map›Paper›PMID 24108187›Full record

ArticlePediatric research2013

Erythropoietin signaling promotes oligodendrocyte development following prenatal systemic hypoxic-ischemic brain injury.

Lauren L Jantzie, Robert H Miller, Shenandoah Robinson

Open access · bronzeAbstract read
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Article in Pediatric research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
13.3field-weighted citation impact, top 1% 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

65 citing papers in PubMed, 119 citations in OpenAlex.

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  10. Anemia, Iron Supplementation, and the Brain.Clinics in perinatology · 2023
    Review
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  12. Recombinant Erythropoietin Induces Oligodendrocyte Progenitor Cell Proliferation After Traumatic Brain Injury and Delayed Hypoxemia.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
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5 more citing papers are in PubMed but not listed here.

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

3 authors at 3 institutions in 1 country.

Lauren L JantzieDepartments of Neurosurgery and Neurology, F.M. Kirby Center for Neurobiology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts.
Robert H MillerDepartment of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, Ohio.
Shenandoah RobinsonDepartments of Neurosurgery and Neurology, F.M. Kirby Center for Neurobiology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts.
Boston Children's Hospital · USCase Western Reserve University · USHarvard University · US

Funding

Mechanisms of Neonatal Erythropoietin NeuroprotectionR01NS060765 · NINDS · CASE WESTERN RESERVE UNIVERSITY · PI ROBINSON, SHENANDOAH · 2008 to 2011
$1.3M
NINDS NIH HHS R01 NS060765NINDS NIH HHS R01-NS060765
6 · The paper itself

Abstract

backgroundBrain injury from preterm birth causes white matter injury (WMI), and it leads to chronic neurological deficits including cerebral palsy, epilepsy, cognitive, and behavioral delay. Immature O4+ oligodendrocytes are particularly vulnerable to WMI. Understanding how the developing brain recovers after injury is essential to finding more effective therapeutic strategies. Erythropoietin (EPO) promotes neuronal recovery after injury; however, its role in enhancing oligodendroglial lineage recovery is unclear. Previously, we found that recombinant EPO (rEPO) treatment enhances myelin basic protein (MBP) expression and functional recovery in adult rats after prenatal transient systemic hypoxia-ischemia (TSHI). We hypothesized that after injury, rEPO would enhance oligodendroglial lineage cell genesis, survival, maturation, and myelination.

methodsIn vitro assays were used to define how rEPO contributes to specific stages of oligodendrocyte development and recovery after TSHI.

resultsAfter prenatal TSHI injury, rEPO promotes genesis of oligodendrocyte progenitors from oligodendrospheres, survival of oligodendrocyte precursor cells (OPCs) and O4+ immature oligodendrocytes, O4+ cell process extension, and MBP expression. rEPO did not alter OPC proliferation.

conclusionTogether, these studies demonstrate that EPO signaling promotes critical stages of oligodendroglial lineage development and recovery after prenatal TSHI injury. EPO treatment may be beneficial to preterm and other infant patient populations with developmental brain injury hallmarked by WMI.

Indexed as

AnimalsBase SequenceBrain InjuriesCell DivisionDNA PrimersErythropoietinFemaleHypoxia-Ischemia, BrainNeurogenesisOligodendrogliaPregnancyRatsRats, Sprague-DawleyRecombinant ProteinsSignal TransductionDNA PrimersErythropoietinRecombinant Proteins

Identifiers

PMID24108187
PMCPMC3865073
OpenAlexW2000198569

What OpenQuestion holds

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Registered trials

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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.