Evidence map›Paper›PMID 25633295›Full record

ArticleCell death & disease2015

Inhibition of immunoproteasome reduces infarction volume and attenuates inflammatory reaction in a rat model of ischemic stroke.

X Chen, X Zhang, Y Wang, H Lei, H Su, J Zeng, Z Pei, R Huang

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 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

41 citing papers in PubMed, 73 citations in OpenAlex.

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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

8 authors at 3 institutions in 2 countries.

X Chen1] Department of Neurology, National Key Clinical Department and Key Discipline of Neurology, Guangdong Key Laboratory for Diagnosis and Treatment of Major Neurological Diseases, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510080, PR China [2] Department of Neurology, Fujian Provincial Hospital, Fujian Medical University Shengli Clinical College, Fuzhou 350001, PR China.
X ZhangDepartment of Neurology, Fujian Provincial Hospital, Fujian Medical University Shengli Clinical College, Fuzhou 350001, PR China.
Y WangDepartment of Neurology, Fujian Provincial Hospital, Fujian Medical University Shengli Clinical College, Fuzhou 350001, PR China.
H LeiDepartment of Neurology, Fujian Provincial Hospital, Fujian Medical University Shengli Clinical College, Fuzhou 350001, PR China.
H SuKey Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, PR China.
J ZengDepartment of Neurology, National Key Clinical Department and Key Discipline of Neurology, Guangdong Key Laboratory for Diagnosis and Treatment of Major Neurological Diseases, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510080, PR China.
Z PeiDepartment of Neurology, National Key Clinical Department and Key Discipline of Neurology, Guangdong Key Laboratory for Diagnosis and Treatment of Major Neurological Diseases, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510080, PR China.
R HuangDepartment of Neurology, National Key Clinical Department and Key Discipline of Neurology, Guangdong Key Laboratory for Diagnosis and Treatment of Major Neurological Diseases, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510080, PR China.
Fujian Provincial Hospital · CNFujian Medical University · CNUniversity of Macau · MO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The detailed knowledge about the contribution of immunoproteasome to the neuroinflammation in ischemic stroke is still not available. The immunoreactivity of low molecular mass peptide 2 (LMP2) and low molecular mass peptide 7 (LMP7) was evident in the ipsilateral ischemic cerebral cortex and striatum following transient middle cerebral artery occlusion (MCAO). Both LMP2 and LMP7 increased as early as 4 h after the MCAO, further increased at 24 h, peaked at 72 h and decreased 7 days later. LMP2 and LMP7 were mainly present in astrocytes and microglia/macrophage cells, respectively. LMP2 knockdown by shRNA (short hairpin RNA) markedly reduced the levels of LMP2 and LMP7 protein and caused 75.5 and 78.6% decrease in the caspase-like (C-L) and chymotrypsin-like (CT-L) activities, respectively. Compared with cont-shRNA group (39.7%, infarction volumes/total ipsilateral hemisphere), the infarction volumes were reduced to 22.5% in LMP2-shRNA group. Additionally, LMP2 knockdown significantly reduced activated astrocytes and microglia, the expression nuclear factor kappa B (NF-κB) p65, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) and caused less accumulation of ischemia-induced protein ubiquitination compared with MG132. These findings demonstrate that inhibition of LMP2 significantly attenuates inflammatory reaction and offers neuroprotection against focal cerebral ischemia in rats, suggesting that selective immunoproteasome inhibitors may be a promising strategy for stroke treatment.

Indexed as

AnimalsAstrocytesCerebral InfarctionCysteine EndopeptidasesDisease Models, AnimalGene Knockdown TechniquesInfarction, Middle Cerebral ArteryInflammationInterleukin-1betaLeupeptinsMaleMicrogliaNF-kappa BProteasome Endopeptidase ComplexProteasome InhibitorsProtein Subunitsbenzyloxycarbonylleucyl-leucyl-leucine aldehydeCysteine EndopeptidasesInterleukin-1betaLeupeptinsLMP-2 proteinLMP7 proteinNF-kappa BProteasome Endopeptidase ComplexProteasome InhibitorsProtein SubunitsRNA, Small InterferingTumor Necrosis Factor-alphaUbiquitinated Proteins

Identifiers

PMID25633295
PMCPMC4669779
OpenAlexW2032884361

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.