Evidence map›Paper›PMID 26858089›Full record

ArticleScientific reports2016

Plumericin inhibits proliferation of vascular smooth muscle cells by blocking STAT3 signaling via S-glutathionylation.

Elke H Heiss, Rongxia Liu, Birgit Waltenberger, Shafaat Khan, Daniel Schachner, Paul Kollmann, Kristin Zimmermann, Muris Cabaravdic, Pavel Uhrin, Hermann Stuppner and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

13 citing papers in PubMed, 27 citations in OpenAlex.

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  5. 7-Biomolecules · 2019
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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

13 authors at 4 institutions in 2 countries.

Elke H HeissDepartment of Pharmacognosy, University of Vienna, Althanstrasse 14, 1090 Vienna, Austria.
Rongxia LiuDepartment of Pharmacognosy, University of Vienna, Althanstrasse 14, 1090 Vienna, Austria.
Birgit WaltenbergerInstitute of Pharmacy (Pharmacognosy) and Center for Molecular Biosciences Innsbruck (CMBI), University of Innsbruck, Innsbruck, Austria.
Shafaat KhanCenter for Physiology and Pharmacology, Institute for Vascular Biology and Thrombosis Research, Medical University of Vienna, Vienna, Austria.
Daniel SchachnerDepartment of Pharmacognosy, University of Vienna, Althanstrasse 14, 1090 Vienna, Austria.
Paul KollmannDepartment of Pharmacognosy, University of Vienna, Althanstrasse 14, 1090 Vienna, Austria.
Kristin ZimmermannDepartment of Pharmacognosy, University of Vienna, Althanstrasse 14, 1090 Vienna, Austria.
Muris CabaravdicCenter for Physiology and Pharmacology, Institute for Vascular Biology and Thrombosis Research, Medical University of Vienna, Vienna, Austria.
Pavel UhrinCenter for Physiology and Pharmacology, Institute for Vascular Biology and Thrombosis Research, Medical University of Vienna, Vienna, Austria.
Hermann StuppnerInstitute of Pharmacy (Pharmacognosy) and Center for Molecular Biosciences Innsbruck (CMBI), University of Innsbruck, Innsbruck, Austria.
Johannes M BreussCenter for Physiology and Pharmacology, Institute for Vascular Biology and Thrombosis Research, Medical University of Vienna, Vienna, Austria.
Atanas G AtanasovDepartment of Pharmacognosy, University of Vienna, Althanstrasse 14, 1090 Vienna, Austria.
Verena M DirschDepartment of Pharmacognosy, University of Vienna, Althanstrasse 14, 1090 Vienna, Austria.
University of Vienna · ATMedical University of Vienna · ATUniversität Innsbruck · ATUniversity of Sargodha · PK

Funding

Austrian Science Fund FWF P 25971Austrian Science Fund FWF S 10703Austrian Science Fund FWF S 10704Austrian Science Fund FWF S 10713
6 · The paper itself

Abstract

The etiology of atherosclerosis and restenosis involves aberrant inflammation and proliferation, rendering compounds with both anti-inflammatory and anti-mitogenic properties as promising candidates for combatting vascular diseases. A recent study identified the iridoid plumericin as a new scaffold inhibitor of the pro-inflammatory NF-κB pathway in endothelial cells. We here examined the impact of plumericin on the proliferation of primary vascular smooth muscle cells (VSMC). Plumericin inhibited serum-stimulated proliferation of rat VSMC. It arrested VSMC in the G1/G0-phase of the cell cycle accompanied by abrogated cyclin D1 expression and hindered Ser 807/811-phosphorylation of retinoblastoma protein. Transient depletion of glutathione by the electrophilic plumericin led to S-glutathionylation as well as hampered Tyr705-phosphorylation and activation of the transcription factor signal transducer and activator of transcription 3 (Stat3). Exogenous addition of glutathione markedly prevented this inhibitory effect of plumericin on Stat3. It also overcame downregulation of cyclin D1 expression and the reduction of biomass increase upon serum exposure. This study revealed an anti-proliferative property of plumericin towards VSMC which depends on plumericin's thiol reactivity and S-glutathionylation of Stat3. Hence, plumericin, by targeting at least two culprits of vascular dysfunction -inflammation and smooth muscle cell proliferation -might become a promising electrophilic lead compound for vascular disease therapy.

Indexed as

AnimalsApocynaceaeCells, CulturedCyclin D1G1 PhaseGlutathioneIndenesIridoidsMuscle, Smooth, VascularMyocytes, Smooth MuscleProtein Processing, Post-TranslationalRatsResting Phase, Cell CycleSignal TransductionSTAT3 Transcription FactorCcnd1 protein, ratCyclin D1GlutathioneIndenesIridoidsplumericinStat3 protein, ratSTAT3 Transcription Factor

Identifiers

PMID26858089
PMCPMC4746734
OpenAlexW2260099822

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.