Evidence map›Paper›PMID 24573298›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

Mir-592 regulates the induction and cell death-promoting activity of p75NTR in neuronal ischemic injury.

Krithi Irmady, Katherine A Jackman, Victoria A Padow, Neelam Shahani, Laura Andres Martin, Leandro Cerchietti, Klaus Unsicker, Costantino Iadecola, Barbara L Hempstead

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

51 citing papers in PubMed, 91 citations in OpenAlex.

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  15. Therapeutic Implications of microRNAs in Depressive Disorders: A Review.International journal of molecular sciences · 2022
    Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. In vivo functions of p75Trends in pharmacological sciences · 2021
    Review
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

9 authors at 4 institutions in 2 countries.

Krithi IrmadyDepartment of Medicine and Brain and Mind Research Institute, Weill Cornell Medical College, New York, New York 10065, and Interdisciplinary Center for Neurosciences, Department of Neuroanatomy, University of Heidelberg, INF 307, D69120 Heidelberg, Germany.
Katherine A Jackman
Victoria A Padow
Neelam Shahani
Laura Andres Martin
Leandro Cerchietti
Klaus Unsicker
Costantino Iadecola
Barbara L Hempstead
MIND Research Institute · USCenter for Neurosciences · USCornell University · USHeidelberg University · DE

Funding

NO SYNTHASE GENE EXPRESSION AND CEREBRAL ISCHEMIC DAMAGER01NS034179 · NINDS · WEILL MEDICAL COLL OF CORNELL UNIV · PI IADECOLA, COSTANTINO · 1995 to 2021
$5.5M
Role of Neurotrophins and Receptors in NeurogenesisR01NS030687 · NINDS · WEILL MEDICAL COLL OF CORNELL UNIV · PI HEMPSTEAD, BARBARA L · 1993 to 2014
$5.1M
CHRONIC INTERMITTENT HYPOXIA, NEUROVASCULAR DYSFUNCTION AND STROKER01NS073666 · NINDS · WEILL MEDICAL COLL OF CORNELL UNIV · PI IADECOLA, COSTANTINO · 2011 to 2015
$1.8M
NO SYNTHASE GENE EXPRESSION AND CEREBRAL ISCHEMIC DAMAGER37NS034179 · NINDS · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI IADECOLA, COSTANTINO · 1999 to 2005
$1.8M
NINDS NIH HHS NS30687NINDS NIH HHS NS34179NINDS NIH HHS NS73666NINDS NIH HHS R01 NS030687NINDS NIH HHS R01 NS034179NINDS NIH HHS R01 NS073666NINDS NIH HHS R37 NS034179
6 · The paper itself

Abstract

The neurotrophin receptor p75(NTR) has been implicated in mediating neuronal apoptosis after injury to the CNS. Despite its frequent induction in pathologic states, there is limited understanding of the mechanisms that regulate p75(NTR) expression after injury. Here, we show that after focal cerebral ischemia in vivo or oxygen-glucose deprivation in organotypic hippocampal slices or neurons, p75(NTR) is rapidly induced. A concomitant induction of proNGF, a ligand for p75(NTR), is also observed. Induction of this ligand/receptor system is pathologically relevant, as a decrease in apoptosis, after oxygen-glucose deprivation, is observed in hippocampal neurons or slices after delivery of function-blocking antibodies to p75(NTR) or proNGF and in p75(NTR) and ngf haploinsufficient slices. Furthermore, a significant decrease in infarct volume was noted in p75(NTR)-/- mice compared with the wild type. We also investigated the regulatory mechanisms that lead to post-ischemic induction of p75(NTR). We demonstrate that induction of p75(NTR) after ischemic injury is independent of transcription but requires active translation. Basal levels of p75(NTR) in neurons are maintained in part by the expression of microRNA miR-592, and an inverse correlation is seen between miR-592 and p75(NTR) levels in the adult brain. After cerebral ischemia, miR-592 levels fall, with a corresponding increase in p75(NTR) levels. Importantly, overexpression of miR-592 in neurons decreases the level of ischemic injury-induced p75(NTR) and attenuates activation of pro-apoptotic signaling and cell death. These results identify miR-592 as a key regulator of p75(NTR) expression and point to a potential therapeutic candidate to limit neuronal apoptosis after ischemic injury.

Indexed as

Age FactorsAnimalsApoptosisDisease Models, AnimalGene Expression RegulationGlucoseHippocampusHumansHypoxiaInfarction, Middle Cerebral ArteryIn Vitro TechniquesMaleMiceMice, Inbred C57BLMice, TransgenicMicroRNAsGlucoseMicroRNAsMIRN592 microRNA, mouseNerve Growth FactorNgfr protein, mousepro-nerve growth factor, mouseProtein PrecursorsReceptors, Nerve Growth FactorRNA, Small InterferingischemiamicroRNAneurotrophinNGFp75NTRstroke

Identifiers

PMID24573298
PMCPMC3935094
OpenAlexW2045122934

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.