Evidence map›Paper›PMID 20919940›Full record

ArticleAntioxidants & redox signaling2011

Oscillatory shear stress induces mitochondrial superoxide production: implication of NADPH oxidase and c-Jun NH2-terminal kinase signaling.

Wakako Takabe, Nelson Jen, Lisong Ai, Ryan Hamilton, Sky Wang, Kristin Holmes, Farhad Dharbandi, Bhavraj Khalsa, Steven Bressler, Mark L Barr and 2 more

Abstract read
In one paragraph

Article in Antioxidants & redox signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

42 citing papers in PubMed, 60 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Permissive role of vascular endothelium in fibrosis: focus on the kidney.American journal of physiology. Cell physiology · 2024
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Modulation of the mitochondrial CaPhysiological reports · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. From Endothelium to Lipids, Through microRNAs and PCSK9: A Fascinating Travel Across Atherosclerosis.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2020
    Review
  17. Review
  18. Article
  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

12 authors at 1 institution in 1 country.

Wakako TakabeDepartment of Biomedical Engineering and Cardiovascular Medicine, University of Southern California, Los Angeles, California 90089, USA.
Nelson Jen
Lisong Ai
Ryan Hamilton
Sky Wang
Kristin Holmes
Farhad Dharbandi
Bhavraj Khalsa
Steven Bressler
Mark L Barr
Rongsong Li
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
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-083015
6 · The paper itself

Abstract

Fluid shear stress is intimately linked with vascular oxidative stress and atherosclerosis. We posited that atherogenic oscillatory shear stress (OSS) induced mitochondrial superoxide (mtO2•-) production via NADPH oxidase and c-Jun NH(2)-terminal kinase (JNK-1 and JNK-2) signaling. In bovine aortic endothelial cells, OSS (±3 dyn/cm2) induced JNK activation, which peaked at 1 h, accompanied by an increase in fluorescein isothiocyanate-conjugated JNK fluorescent and MitoSOX Red (specific for mtO2•- production) intensities. Pretreatment with apocynin (NADPH oxidase inhibitor) or N-acetyl cysteine (antioxidant) significantly attenuated OSS-induced JNK activation. Apocynin further reduced OSS-mediated dihydroethidium and MitoSOX Red intensities specific for cytosolic O2•- and mtO2•- production, respectively. As a corollary, transfecting bovine aortic endothelial cells with JNK siRNA (siJNK) and pretreating with SP600125 (JNK inhibitor) significantly attenuated OSS-mediated mtO2•- production. Immunohistochemistry on explants of human coronary arteries further revealed prominent phosphorylated JNK staining in OSS-exposed regions. These findings indicate that OSS induces mtO2•- production via NADPH oxidase and JNK activation relevant for vascular oxidative stress.

Indexed as

Stress, MechanicalAnimalsCattleCoronary VesselsCytosolEndothelial CellsEnzyme ActivationGene Expression RegulationGene Knockdown TechniquesHemodynamicsHumansJNK Mitogen-Activated Protein KinasesMitochondriaNADPH OxidasesOxidative StressShear StrengthJNK Mitogen-Activated Protein KinasesNADPH OxidasesSuperoxides

Identifiers

PMID20919940
PMCPMC3144427
OpenAlexW2038104990

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.