Evidence map›Paper›PMID 25675298›Full record

ArticleCell death & disease2015

Prolyl hydroxylase regulates axonal rewiring and motor recovery after traumatic brain injury.

S Miyake, R Muramatsu, M Hamaguchi, T Yamashita

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
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  6. Review
  7. Article
  8. Transient Hypoxemia Chronically Disrupts Maturation of Preterm Fetal Ovine Subplate Neuron Arborization and Activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  9. 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

4 authors at 1 institution in 1 country.

S Miyake1] Department of Molecular Neuroscience, Graduate school of Medicine, Osaka University, Suita, Osaka, Japan [2] Japan Science and Technology Agency, Core Research for Evolutional Science and Technology, Chiyoda, Tokyo, Japan.
R Muramatsu1] Department of Molecular Neuroscience, Graduate school of Medicine, Osaka University, Suita, Osaka, Japan [2] Japan Science and Technology Agency, Core Research for Evolutional Science and Technology, Chiyoda, Tokyo, Japan [3] Precursory Research for Embryonic Science and Technology, Japan Science and Technology Agency, 5, Sanbancho, Chiyoda-ku, Tokyo, Japan.
M Hamaguchi1] Department of Molecular Neuroscience, Graduate school of Medicine, Osaka University, Suita, Osaka, Japan [2] Japan Science and Technology Agency, Core Research for Evolutional Science and Technology, Chiyoda, Tokyo, Japan.
T Yamashita1] Department of Molecular Neuroscience, Graduate school of Medicine, Osaka University, Suita, Osaka, Japan [2] Japan Science and Technology Agency, Core Research for Evolutional Science and Technology, Chiyoda, Tokyo, Japan.
Osaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prolyl 4-hydroxylases (PHDs; PHD1, PHD2, and PHD3) are a component of cellular oxygen sensors that regulate the adaptive response depending on the oxygen concentration stabilized by hypoxia/stress-regulated genes transcription. In normoxic condition, PHD2 is required to stabilize hypoxia inducible factors. Silencing of PHD2 leads to the activation of intracellular signaling including RhoA and Rho-associated protein kinase (ROCK), which are key regulators of neurite growth. In this study, we determined that genetic or pharmacological inhibition of PHD2 in cultured cortical neurons prevents neurite elongation through a ROCK-dependent mechanism. We then explored the role of PHDs in axonal reorganization following a traumatic brain injury in adult mice. Unilateral destruction of motor cortex resulted in behavioral deficits due to disruption of the corticospinal tract (CST), a part of the descending motor pathway. In the spinal cord, sprouting of fibers from the intact side of the CST into the denervated side is thought to contribute to the recovery process following an injury. Intracortical infusion of PHD inhibitors into the intact side of the motor cortex abrogated spontaneous formation of CST collaterals and functional recovery after damage to the sensorimotor cortex. These findings suggest PHDs have an important role in the formation of compensatory axonal networks following an injury and may represent a new molecular target for the central nervous system disorders.

Indexed as

AnimalsAxonsBrain InjuriesCells, CulturedHypoxia-Inducible Factor-Proline DioxygenasesMiceMice, Inbred C57BLNeuritesNeuronsProlyl HydroxylasesPyramidal TractsRecovery of Functionrho-Associated KinasesEgln1 protein, mouseHypoxia-Inducible Factor-Proline DioxygenasesProlyl Hydroxylasesrho-Associated Kinases

Identifiers

PMID25675298
PMCPMC4669805
OpenAlexW2077524574

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.