Evidence map›Paper›PMID 24713818›Full record

ArticlePediatric research2014

Hypoxic preconditioning protection is eliminated in HIF-1α knockout mice subjected to neonatal hypoxia-ischemia.

R Ann Sheldon, Christina L Lee, Xiangning Jiang, Renatta N Knox, Donna M Ferriero

Open access · bronzeAbstract read
In one paragraph

Article in Pediatric research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
9.1field-weighted citation impact, top 2% 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

28 citing papers in PubMed, 54 citations in OpenAlex.

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  13. Glucocorticoid-Dependent Mechanisms of Brain Tolerance to Hypoxia.International journal of molecular sciences · 2021
    Review
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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

5 authors at 1 institution in 1 country.

R Ann Sheldon1] Department of Pediatrics, University of California, San Francisco, San Francisco, California [2] Newborn Brain Research Institute, University of California, San Francisco, San Francisco, California.
Christina L LeeDepartment of Pediatrics, University of California, San Francisco, San Francisco, California.
Xiangning Jiang1] Department of Pediatrics, University of California, San Francisco, San Francisco, California [2] Newborn Brain Research Institute, University of California, San Francisco, San Francisco, California.
Renatta N KnoxDepartment of Pediatrics, University of California, San Francisco, San Francisco, California.
Donna M Ferriero1] Department of Pediatrics, University of California, San Francisco, San Francisco, California [2] Newborn Brain Research Institute, University of California, San Francisco, San Francisco, California [3] Department of Neurology, University of California, San Francisco, San Francisco, California.
University of California, San Francisco · US

Funding

Oxidant Mechanisms in Neonatal Brain InjuryR01NS033997 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI FERRIERO, DONNA M. · 1996 to 2016
$5.1M
Phospho-regulation of NMDA receptors in neonatal brain hypoxia-ischemiaR01NS084057 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JIANG, XIANGNING · 2014 to 2018
$1.7M
NINDS NIH HHS R01 NS033997NINDS NIH HHS R01 NS084057
6 · The paper itself

Abstract

backgroundHypoxic preconditioning (HPc) protects the neonatal brain in the setting of hypoxia-ischemia (HI). The mechanisms of protection may depend on activation of hypoxia-inducible factor (HIF-1α). This study sought to clarify the role of HIF-1α after HPc and HI.

methodsTo induce HPc, HIF-1α knockout and wild-type (WT) mice were exposed to hypoxia at postnatal day 6. At day 7, the mice underwent HI. Brain injury was determined by histology. HIF-1α, downstream targets, and markers of cell death were measured by western blot.

resultsHPc protected the WT brain compared with WT without HPc, but did not protect the HIF-1α knockout brain. In WT, HIF-1α increased after hypoxia and after HI, but not with HPc. The HIF-1α knockout showed no change in HIF-1α after hypoxia, HI, or HPc/HI. After HI, spectrin 145/150 was higher in HIF-1α knockout, but after HPc/HI, it was higher in WT. Lysosome-associated membrane protein was higher in WT early after HI, but not later. After HPc/HI, lysosome-associated membrane protein was higher in HIF-1α knockout.

conclusionThese results indicate that HIF-1α is necessary for HPc protection in the neonatal brain and may affect cell death after HI. Different death and repair mechanisms depend on the timing of HPc.

Indexed as

AnimalsAnimals, NewbornApoptosisBrainBrain InjuriesCell DeathExtracellular Signal-Regulated MAP KinasesFemaleGenotypeHypoxiaHypoxia-Inducible Factor 1, alpha SubunitHypoxia-Ischemia, BrainIschemic PreconditioningLysosomal Membrane ProteinsMaleMiceExtracellular Signal-Regulated MAP KinasesHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitLysosomal Membrane ProteinsSpectrinVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouse

Identifiers

PMID24713818
PMCPMC4167022
OpenAlexW2084977349

What OpenQuestion holds

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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.