Evidence map›Paper›PMID 25015774›Full record

ArticleAge (Dordrecht, Netherlands)2014

ERK5/KLF4 signaling as a common mediator of the neuroprotective effects of both nerve growth factor and hydrogen peroxide preconditioning.

Chang Su, Fen Sun, Rebecca L Cunningham, Nataliya Rybalchenko, Meharvan Singh

Open access · bronzeAbstract read
In one paragraph

Article in Age (Dordrecht, Netherlands), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

27 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Effect of Kruppel-like factor 4 on PTZ-induced acute seizure mice.Journal of cellular and molecular medicine · 2024
    Article
  5. Review
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  7. Review
  8. Transcription factors are potential therapeutic targets in epilepsy.Journal of cellular and molecular medicine · 2022
    Review
  9. Article
  10. Article
  11. Review
  12. Distinct peripheral blood monocyte and neutrophil transcriptional programs following intracerebral hemorrhage and different etiologies of ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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 2 institutions in 1 country.

Chang SuDepartment of Pharmacology and Neuroscience, University of North Texas Health Science Center, Fort Worth, TX, 76107, USA, Chang.Su@unthsc.edu.
Fen Sun
Rebecca L Cunningham
Nataliya Rybalchenko
Meharvan Singh
University of North Texas · USUniversity of North Texas Health Science Center · US

Funding

Protein Targets of Oxidative Brain AgingP01AG022550 · NIA · WEST VIRGINIA UNIVERSITY · PI SIMPKINS, JAMES W. · 2003 to 2013
$15.7M
ROLE OF MITHOCHONDRIAL ERB IN NEURONAL VULNDERABILITY TO NEUROTOXIC STRESSP01AG027956 · NIA · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI SINGH, MEHARVAN · 2007 to 2017
$11.3M
NIA NIH HHS AG022550NIA NIH HHS AG027956NIA NIH HHS P01 AG022550NIA NIH HHS P01 AG027956
6 · The paper itself

Abstract

Oxidative stress has long been implicated in the pathogenesis of various neurodegenerative disorders such as Alzheimer's disease and stroke. While high levels of oxidative stress are generally associated with cell death, a slight rise of reactive oxygen species (ROS) levels can be protective by "preconditioning" cells to develop a resistance against subsequent challenges. However, the mechanisms underlying such preconditioning (PC)-induced protection are still poorly understood. Previous studies have supported a role of ERK5 (mitogen-activated protein [MAP] kinase 5) in neuroprotection and ischemic tolerance in the hippocampus. In agreement with these findings, our data suggest that ERK5 mediates both hydrogen peroxide (H2O2)-induced PC as well as nerve growth factor (NGF)-induced neuroprotection. Activation of ERK5 partially rescued pheochromocytoma PC12 cells as well as primary hippocampal neurons from H2O2-caused death, while inhibition of ERK5 abolished NGF or PC-induced protection. These results implicate ERK5 signaling as a common downstream pathway for NGF and PC. Furthermore, both NGF and PC increased the expression of the transcription factor, KLF4, which can initiate an anti-apoptotic response in various cell types. Induction of KLF4 by NGF or PC was blocked by siERK5, suggesting that ERK5 is required in this process. siKLF4 can also attenuate NGF- or PC-induced neuroprotection. Overexpression of active MEK5 or KLF4 in H2O2-stressed cells increased Bcl-2/Bax ratio and the expression of NAIP (neuronal apoptosis inhibitory protein). Taken together, our data suggest that ERK5/KLF4 cascade is a common signaling pathway shared by at least two important mechanisms by which neurons can be protected from cell death.

Indexed as

ApoptosisGene Expression RegulationAnimalsBlotting, WesternCells, CulturedHippocampusHydrogen PeroxideKruppel-Like Factor 4Kruppel-Like Transcription FactorsMiceMitogen-Activated Protein Kinase 7Nerve Growth FactorNeurodegenerative DiseasesNeuroprotective AgentsOxidative StressRatsHydrogen PeroxideKlf4 protein, mouseKlf4 protein, ratKruppel-Like Factor 4Kruppel-Like Transcription FactorsMitogen-Activated Protein Kinase 7Nerve Growth FactorNeuroprotective AgentsRNA

Identifiers

PMID25015774
PMCPMC4150906
OpenAlexW2028890185

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.