Evidence map›Paper›PMID 20139358›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2010

Oxidized low-density lipoprotein-activated c-Jun NH2-terminal kinase regulates manganese superoxide dismutase ubiquitination: implication for mitochondrial redox status and apoptosis.

Wakako Takabe, Rongsong Li, Lisong Ai, Fei Yu, Judith A Berliner, Tzung K Hsiai

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

30 citing papers in PubMed, 57 citations in OpenAlex.

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  13. The metabolic syndrome and chronic kidney disease.Translational research : the journal of laboratory and clinical medicine · 2017
    Review
  14. Article
  15. Article
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  18. Article
  19. Blood flow modulation of vascular dynamics.Current opinion in lipidology · 2015
    Review
  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

6 authors at 1 institution in 1 country.

Wakako TakabeDepartment of Biomedical Engineering and Division of Cardiovascular Medicine, School of Medicine and School of Engineering, University of Southern California, 1042 Downey Way, Los Angeles, CA 90089, USA.
Rongsong Li
Lisong Ai
Fei Yu
Judith A Berliner
Tzung K Hsiai
University of Southern California · US

Funding

Linking Spatial Variations Shear Stress-Oxidative StressR01HL083015 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HSIAI, TZUNG K · 2006 to 2015
$3.9M
Electronica Impedance to Access Metabolically Active PlaqueR01HL118650 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI HSIAI, TZUNG K · 2014 to 2022
$3.3M
Microsensors to Study Endothelial Cell DynamicsK08HL068689 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HSIAI, TZUNG K · 2003 to 2007
$514k
NHLBI NIH HHS HL-068689NHLBI NIH HHS HL-083015NHLBI NIH HHS K08 HL068689NHLBI NIH HHS R01 HL083015NHLBI NIH HHS R01 HL118650
6 · The paper itself

Abstract

objectiveOxidized low-density lipoprotein (oxLDL) modulates intracellular redox status and induces apoptosis in endothelial cells. However, the signal pathways and molecular mechanism remain unknown. In this study, we investigated the role of manganese superoxide dismutase (Mn-SOD) on oxLDL-induced apoptosis via c-Jun NH2-terminal kinase (JNK)-mediated ubiquitin/proteasome pathway. METHODS AND

resultsOxLDL induced JNK phosphorylation that peaked at 30 minutes in human aortic endothelial cells. Fluorescence-activated cell sorting analysis revealed that oxLDL increased mitochondrial superoxide production by 1.88+/-0.19-fold and mitochondrial membrane potential by 18%. JNK small interference RNA (siJNK) reduced oxLDL-induced mitochondrial superoxide production by 88.4% and mitochondrial membrane potential by 61.7%. OxLDL did not affect Mn-SOD mRNA expression, but it significantly reduced Mn-SOD protein level, which was restored by siJNK. Immunoprecipitation by ubiquitin antibody revealed that oxLDL increased ubiquitination of Mn-SOD, which was inhibited by siJNK. OxLDL-induced caspase-3 activities were also attenuated by siJNK but were enhanced by Mn-SOD small interfering RNA. Furthermore, overexpression of Mn-SOD abrogated oxLDL-induced caspase-3 activities.

conclusionsOxLDL-induced JNK activation regulates mitochondrial redox status and Mn-SOD protein degradation via JNK-dependent ubiquitination, leading to endothelial cell apoptosis.

Indexed as

AortaApoptosisCaspase 3Cells, CulturedEndothelium, VascularHumansJNK Mitogen-Activated Protein KinasesLipoproteins, LDLMembrane Potential, MitochondrialMitochondriaOxidation-ReductionProteasome Endopeptidase ComplexSignal TransductionSuperoxide DismutaseUbiquitinationCaspase 3JNK Mitogen-Activated Protein KinasesLipoproteins, LDLoxidized low density lipoproteinProteasome Endopeptidase ComplexSuperoxide Dismutase

Identifiers

PMID20139358
PMCPMC3324126
OpenAlexW1975302485

What OpenQuestion holds

Textmetadata
LicenceTDM
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.