Evidence map›Paper›PMID 23826409›Full record

ArticleInternational journal of clinical and experimental pathology2013

Dynamic change of SGK expression and its role in neuron apoptosis after traumatic brain injury.

Xinmin Wu, Hui Mao, Jiao Liu, Jian Xu, Jianhua Cao, Xingxing Gu, Gang Cui

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Review
  6. Axonal and Myelin Neuroprotection by the Peptoid BN201 in Brain Inflammation.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019
    Article
  7. Article
  8. Article
  9. Up-regulation of Wnt/β-catenin expression is accompanied with vascular repair after traumatic brain injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018
    Article
  10. Response of the cerebral vasculature following traumatic brain injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. 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

7 authors at 1 institution in 1 country.

Xinmin WuDepartment of Neurology, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province 226001, People's Republic of China.
Hui Mao
Jiao Liu
Jian Xu
Jianhua Cao
Xingxing Gu
Gang Cui
Nantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsActivation of specific signaling pathways in response to mechanical trauma causes delayed neuronal apoptosis; GSK-3β/β-catenin signaling plays a critical role in the apoptosis of neurons in CNS diseases, SGK was discovered as a regulator of GSK-3β/β-catenin pathway, The goal of this study was to determine if the mechanism of cell death or survival mediated by the SGK/GSK-3β/β-catenin pathway is involved in a rat model of TBI. MAIN

methodsHere, an acute traumatic brain injury model was applied to investigate the expression change and possible roles of SGK, Expression of SGK, and total-GSK-3β, phospho-GSK3β on ser-9, beta-catenin, and caspase-3 were examined by immunohistochemistry and Western blot analysis. Double immunofluorescent staining was used to observe the SGK localizations. Si-RNA was performed to identify whether SGK regulates neuron apoptosis via GSK-3β/β-catenin pathway, ultimately inhibit caspase-3 activation. KEY

findingsTemporally, SGK expression showed an increase pattern after TBI and reached a peak at day 3. Spatially, SGK was widely expressed in the neuron, rarely in astrocytes and oligodendrocytes; in addition, the expression patterns of active caspase-3 and phospho-GSK3β were parallel with that of SGK, at the same time, the expression of β-catenin shows similarity with SGK. In vitro, to further investigate the function of SGK, a neuronal cell line PC12 was employed to establish an apoptosis model. We analyzed the association of SGK with apoptosis on PC12 cells by western blot, immunofluorescent labeling and siRNA. SIGNIFICANCE: the results implied that SGK plays an important role in neuron apoptosis via the regulation of GSK3β/β-catenin signaling pathway; ultimately inhibit caspase-3 activation. Taken together, we inferred traumatic brain injury induced an upregulation of SGK in the central nervous system, which show a protective role in neuron apoptosis.

Indexed as

ApoptosisAnimalsbeta CateninBrainBrain InjuriesCaspase 3Disease Models, AnimalGene Expression Regulation, EnzymologicGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaImmediate-Early ProteinsMaleNeuronsPC12 CellsPhosphorylationProtein Serine-Threonine Kinasesbeta CateninCasp3 protein, ratCaspase 3Ctnnb1 protein, ratGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, ratImmediate-Early ProteinsProtein Serine-Threonine KinasesRNA, MessengerSerum-Glucocorticoid Regulated KinasesGSK3β/β-catenin signaling pathwayneuron apoptosisSGKtraumatic brain injury (TBI)

Identifiers

PMID23826409
PMCPMC3693193
OpenAlexW1562328250

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.