Evidence map›Paper›PMID 24725826›Full record

ArticleJournal of cellular and molecular medicine2014

PMC, a potent hydrophilic α-tocopherol derivative, inhibits NF-κB activation via PP2A but not IκBα-dependent signals in vascular smooth muscle cells.

Cheng-Ying Hsieh, George Hsiao, Ming-Jen Hsu, Yi-Hsuan Wang, Joen-Rong Sheu

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

7 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. Role of protein phosphatase 2A in kidney disease (Review).Experimental and therapeutic medicine · 2021
    Review
  4. Article
  5. Review
  6. Article
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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

5 authors at 1 institution in 1 country.

Cheng-Ying HsiehDepartment of Pharmacology, School of Medicine, Taipei Medical University, Taipei, Taiwan.
George Hsiao
Ming-Jen Hsu
Yi-Hsuan Wang
Joen-Rong Sheu
Taipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The hydrophilic α-tocopherol derivative, 2,2,5,7,8-pentamethyl-6-hydroxychromane (PMC), is a promising alternative to vitamin E in clinical applications. Critical vascular inflammation leads to vascular dysfunction and vascular diseases, including atherosclerosis, hypertension and abdominal aortic aneurysms. In this study, we investigated the mechanisms of the inhibitory effects of PMC in vascular smooth muscle cells (VSMCs) exposed to pro-inflammatory stimuli, lipopolysaccharide (LPS) combined with interferon (IFN)-γ. Treatment of LPS/IFN-γ-stimulated VSMCs with PMC suppressed the expression of inducible nitric oxide synthase (iNOS) and matrix metalloproteinase-9 in a concentration-dependent manner. A reduction in LPS/IFN-γ-induced nuclear factor (NF)-κB activation was also observed in PMC-treated VSMCs. The translocation and phosphorylation of p65, protein phosphatase 2A (PP2A) inactivation and the formation of reactive oxygen species (ROS) were significantly inhibited by PMC in LPS/IFN-γ-activated VSMCs. However, neither IκBα degradation nor IκB kinase (IKK) or ribosomal s6 kinase-1 phosphorylation was affected by PMC under these conditions. Both treatments with okadaic acid, a PP2A-selective inhibitor, and transfection with PP2A siRNA markedly reversed the PMC-mediated inhibition of iNOS expression, NF-κB-promoter activity and p65 phosphorylation. Immunoprecipitation analysis of the cellular extracts of LPS/IFN-γ-stimulated VSMCs revealed that p65 colocalizes with PP2A. In addition, p65 phosphorylation and PP2A inactivation were induced in VSMCs by treatment with H(2)O(2), but neither IκBα degradation nor IKK phosphorylation was observed. These results collectively indicate that the PMC-mediated inhibition of NF-κB activity in LPS/IFN-γ-stimulated VSMCs occurs through the ROS-PP2A-p65 signalling cascade, an IKK-IκBα-independent mechanism. Therapeutic interventions using PMC may therefore be beneficial for the treatment of vascular inflammatory diseases.

Indexed as

AnimalsBenzopyransBlotting, WesternCell ProliferationCells, CulturedFluorescent Antibody TechniqueHydrogen PeroxideI-kappa B KinaseI-kappa B ProteinsImmunoprecipitationInterferon-gammaLipopolysaccharidesMaleMicroscopy, ConfocalMuscle, Smooth, VascularNF-kappa B2,2,5,7,8-pentamethyl-6-hydroxychromaneBenzopyransHydrogen PeroxideI-kappa B KinaseI-kappa B ProteinsInterferon-gammaLipopolysaccharidesNF-kappa BNF-KappaB Inhibitor alphaNfkbia protein, ratNitric OxideNitric Oxide Synthase Type IIOxidantsProtein Phosphatase 2Reactive Oxygen SpeciesRNA, Small InterferingNF-κBPMCPP2AROSvascular inflammation

Identifiers

PMID24725826
PMCPMC4124013
OpenAlexW2093226733

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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.