Evidence map›Paper›PMID 21557011›Full record

ArticleBasic research in cardiology2011

Glycogen synthase kinase 3 beta positively regulates Notch signaling in vascular smooth muscle cells: role in cell proliferation and survival.

Shaunta Guha, John P Cullen, David Morrow, Alberto Colombo, Caitríona Lally, Dermot Walls, Eileen M Redmond, Paul A Cahill

Abstract read
In one paragraph

Article in Basic research in cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

26 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
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  5. Deciphering Molecular Mechanisms Governing the Reproductive Molt ofInternational journal of molecular sciences · 2023
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  14. PI5P4Kγ functions in DTX1-mediated Notch signaling.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  15. 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

8 authors at 2 institutions in 2 countries.

Shaunta GuhaVascular Health Research Centre, Faculty of Science and Health, Dublin City University, Dublin 9, Ireland.
John P Cullen
David Morrow
Alberto Colombo
Caitríona Lally
Dermot Walls
Eileen M Redmond
Paul A Cahill
Dublin City University · IEUniversity of Rochester Medical Center · US

Funding

ALCOHOL REGULATION OF SMOOTH MUSCLE MIGRATION AND GROWTHR01AA012610 · NIAAA · UNIVERSITY OF ROCHESTER · PI REDMOND, EILEEN M. · 1999 to 2008
$2.4M
Pulsatile Flow Regulation of Vascular Cell FateK99HL095650 · NHLBI · UNIVERSITY OF ROCHESTER · PI MORROW, DAVID JOHN · 2009 to 2010
$194k
NHLBI NIH HHS K99 HL095650NHLBI NIH HHS K99HL095650NIAAA NIH HHS AA-12610NIAAA NIH HHS R01 AA012610
6 · The paper itself

Abstract

The role of glycogen synthase kinase 3 beta (GSK-3β) in modulating Notch control of vascular smooth muscle cell (vSMC) growth (proliferation and apoptosis) was examined in vitro under varying conditions of cyclic strain and validated in vivo following changes in medial tension and stress. Modulation of GSK-3β in vSMC following ectopic expression of constitutively active GSK-3β, siRNA knockdown and pharmacological inhibition with SB-216763 demonstrated that GSK-3β positively regulates Notch intracellular domain expression, CBF-1/RBP-Jκ transactivation and downstream target gene mRNA levels, while concomitantly promoting vSMC proliferation and inhibiting apoptosis. In contrast, inhibition of GSK-3β attenuated Notch signaling and decreased vSMC proliferation and survival. Exposure of vSMC to cyclic strain environments in vitro using both a Flexercell™ Tension system and a novel Sylgard™ phantom vessel following bare metal stent implantation revealed that cyclic strain inhibits GSK-3β activity independent of p42/p44 MAPK and p38 activation concomitant with reduced Notch signaling and decreased vSMC proliferation and survival. Exposure of vSMC to changes in medial strain microenvironments in vivo following carotid artery ligation revealed that enhanced GSK-3β activity was predominantly localized to medial and neointimal vSMC concomitant with increased Notch signaling, proliferating nuclear antigen and decreased Bax expression, respectively, as vascular remodeling progressed. GSK-3β is an important modulator of Notch signaling leading to altered vSMC cell growth where low strain/tension microenvironments prevail.

Indexed as

Cell ProliferationAnimalsApoptosisBiomechanical PhenomenaCells, CulturedCell SurvivalGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaMiceModels, AnimalMuscle, Smooth, VascularNeointimaRatsReceptors, NotchSignal TransductionGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, mouseGsk3b protein, ratReceptors, Notch

Identifiers

PMID21557011
PMCPMC3377369
OpenAlexW1964367654

What OpenQuestion holds

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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.