Evidence map›Paper›PMID 24722771›Full record

ArticleCerebral cortex (New York, N.Y. : 1991)2015

Postnatal Erythropoietin Mitigates Impaired Cerebral Cortical Development Following Subplate Loss from Prenatal Hypoxia-Ischemia.

Lauren L Jantzie, Christopher J Corbett, Daniel J Firl, Shenandoah Robinson

Open access · bronzeAbstract read
In one paragraph

Article in Cerebral cortex (New York, N.Y. : 1991), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
13.7field-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

48 citing papers in PubMed, 76 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Lauren L JantzieDepartment of Neurosurgery, Kirby Center for Neurobiology, Boston Children's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Christopher J CorbettDepartment of Neurosurgery, Kirby Center for Neurobiology, Boston Children's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Daniel J FirlDepartment of Neurosurgery, Kirby Center for Neurobiology, Boston Children's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Shenandoah RobinsonDepartment of Neurosurgery, Kirby Center for Neurobiology, Boston Children's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Boston Children's Hospital · USHarvard University · US

Funding

SYNAPTIC MECHANISMS IN HIPPOCAMPAL EPILEPTOGENESISP30HD018655 · NICHD · CHILDREN'S HOSPITAL BOSTON · PI POMEROY, SCOTT LOREN · 1985 to 2015
$26.2M
Integrative Program in CNS Pathophysiology ResearchP30GM103400 · NIGMS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI LIU, KE JIAN · 2012 to 2016
$4.7M
NICHD NIH HHS P30 HD018655NIGMS NIH HHS P30 GM103400
6 · The paper itself

Abstract

Preterm birth impacts brain development and leads to chronic deficits including cognitive delay, behavioral problems, and epilepsy. Premature loss of the subplate, a transient subcortical layer that guides development of the cerebral cortex and axonal refinement, has been implicated in these neurological disorders. Subplate neurons influence postnatal upregulation of the potassium chloride co-transporter KCC2 and maturation of γ-amino-butyric acid A receptor (GABAAR) subunits. We hypothesized that prenatal transient systemic hypoxia-ischemia (TSHI) in Sprague-Dawley rats that mimic brain injury from extreme prematurity in humans would cause premature subplate loss and affect cortical layer IV development. Further, we predicted that the neuroprotective agent erythropoietin (EPO) could attenuate the injury. Prenatal TSHI induced subplate neuronal loss via apoptosis. TSHI impaired cortical layer IV postnatal upregulation of KCC2 and GABAAR subunits, and postnatal EPO treatment mitigated the loss (n ≥ 8). To specifically address how subplate loss affects cortical development, we used in vitro mechanical subplate ablation in slice cultures (n ≥ 3) and found EPO treatment attenuates KCC2 loss. Together, these results show that subplate loss contributes to impaired cerebral development, and EPO treatment diminishes the damage. Limitation of premature subplate loss and the resultant impaired cortical development may minimize cerebral deficits suffered by extremely preterm infants.

Indexed as

Cerebral CortexAge FactorsAnimalsAnimals, NewbornBrain InjuriesCell DeathDisease Models, AnimalEmbryo, MammalianErythropoietinFetal DiseasesGene Expression Regulation, DevelopmentalHypoxia-Ischemia, BrainIn Vitro TechniquesK Cl- CotransportersMotor ActivityNuclear Receptor Subfamily 4, Group A, Member 2ErythropoietinK Cl- CotransportersNr4a2 protein, ratNuclear Receptor Subfamily 4, Group A, Member 2Receptors, GABA-ASymportersdevelopmentGABA receptorKCC2prematuritysubplatethalamocorticalwhite matter

Identifiers

PMID24722771
PMCPMC4537428
OpenAlexW2029804074

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.