Evidence map›Paper›PMID 28726275›Full record

ArticleJournal of cellular and molecular medicine2017

cPKCγ-mediated down-regulation of UCHL1 alleviates ischaemic neuronal injuries by decreasing autophagy via ERK-mTOR pathway.

Dan Zhang, Song Han, Shizun Wang, Yanlin Luo, Li Zhao, Junfa Li

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 31 citations in OpenAlex.

  1. Metabolic Imaging and Molecular Signatures Reveal Metabolic Phenotypes in Recurrent Glioblastoma.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2026
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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

6 authors at 1 institution in 1 country.

Dan ZhangDepartment of Neurobiology and Center of Stroke, Beijing Institute for Brain Disorders, Capital Medical University, Beijing, China.
Song HanDepartment of Neurobiology and Center of Stroke, Beijing Institute for Brain Disorders, Capital Medical University, Beijing, China.
Shizun WangDepartment of Neurobiology and Center of Stroke, Beijing Institute for Brain Disorders, Capital Medical University, Beijing, China.
Yanlin LuoDepartment of Neurobiology and Center of Stroke, Beijing Institute for Brain Disorders, Capital Medical University, Beijing, China.
Li ZhaoDepartment of Neurobiology and Center of Stroke, Beijing Institute for Brain Disorders, Capital Medical University, Beijing, China.ORCID http://orcid.org/0000-0002-2578-9533
Junfa LiDepartment of Neurobiology and Center of Stroke, Beijing Institute for Brain Disorders, Capital Medical University, Beijing, China.ORCID http://orcid.org/0000-0002-1930-9724
Capital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stroke is one of the leading causes of death in the world, but its underlying mechanisms remain unclear. Both conventional protein kinase C (cPKC)γ and ubiquitin C-terminal hydrolase L1 (UCHL1) are neuron-specific proteins. In the models of 1-hr middle cerebral artery occlusion (MCAO)/24-hr reperfusion in mice and 1-hr oxygen-glucose deprivation (OGD)/24-hr reoxygenation in cortical neurons, we found that cPKCγ gene knockout remarkably aggravated ischaemic injuries and simultaneously increased the levels of cleaved (Cl)-caspase-3 and LC3-I proteolysis product LC3-II, and the ratio of TUNEL-positive cells to total neurons. Moreover, cPKCγ gene knockout could increase UCHL1 protein expression via elevating its mRNA level regulated by the nuclear factor κB inhibitor alpha (IκB-α)/nuclear factor κB (NF-κB) pathway in cortical neurons. Both inhibitor and shRNA of UCHL1 significantly reduced the ratio of LC3-II/total LC3, which contributed to neuronal survival after ischaemic stroke, but did not alter the level of Cl-caspase-3. In addition, UCHL1 shRNA reversed the effect of cPKCγ on the phosphorylation levels of mTOR and ERK rather than that of AMPK and GSK-3β. In conclusion, our results suggest that cPKCγ activation alleviates ischaemic injuries of mice and cortical neurons through inhibiting UCHL1 expression, which may negatively regulate autophagy through ERK-mTOR pathway.

Indexed as

AnimalsAutophagyCaspase 3Cell SurvivalCerebral ArteriesCerebral CortexCerebrovascular DisordersDisease Models, AnimalGene Expression RegulationGlucoseMaleMiceMice, KnockoutMicrotubule-Associated ProteinsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Casp3 protein, mouseCaspase 3GlucoseMap1lc3b protein, mouseMapk1 protein, mouseMicrotubule-Associated ProteinsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3mTOR protein, mouseNF-KappaB Inhibitor alphaOxygenProtein IsoformsProtein Kinase Cprotein kinase C gammaRNA, Small InterferingTOR Serine-Threonine KinasesUbiquitin ThiolesteraseUchl1 protein, mouseautophagyconventional protein kinase C (cPKC)γextracellular signal-regulated kinaseischaemic strokemammalian target of rapamycinubiquitin C-terminal hydrolase L1

Identifiers

PMID28726275
PMCPMC5706506
OpenAlexW2737175394

What OpenQuestion holds

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Registered trials

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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.