Evidence map›Paper›PMID 27013612›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2016

The Actin-Binding Protein Drebrin Inhibits Neointimal Hyperplasia.

Jonathan A Stiber, Jiao-Hui Wu, Lisheng Zhang, Igor Nepliouev, Zhu-Shan Zhang, Victoria G Bryson, Leigh Brian, Rex C Bentley, Phillip R Gordon-Weeks, Paul B Rosenberg and 1 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

9 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Drebrin Regulates Collateral Axon Branching in Cortical Layer II/III Somatosensory Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  4. Article
  5. Article
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  7. Article
  8. Article
  9. Reporting Sex and Sex Differences in Preclinical Studies.Arteriosclerosis, thrombosis, and vascular biology · 2018
    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

11 authors at 2 institutions in 1 country.

Jonathan A StiberFrom the Department of Medicine, Duke University Medical Center, Durham, NC (J.A.S., J.-H.W., L.Z., I.N., Z.-S.Z., V.G.B., L.B., P.B.R., N.J.F.); Department of Pathology, Duke University Medical Center, Durham, NC (R.C.B.); and MRC Centre for Developmental Neurobiology, King's College, London, UK (P.R.G.-W.). stibe001@mc.duke.edu.
Jiao-Hui WuFrom the Department of Medicine, Duke University Medical Center, Durham, NC (J.A.S., J.-H.W., L.Z., I.N., Z.-S.Z., V.G.B., L.B., P.B.R., N.J.F.); Department of Pathology, Duke University Medical Center, Durham, NC (R.C.B.); and MRC Centre for Developmental Neurobiology, King's College, London, UK (P.R.G.-W.).
Lisheng ZhangFrom the Department of Medicine, Duke University Medical Center, Durham, NC (J.A.S., J.-H.W., L.Z., I.N., Z.-S.Z., V.G.B., L.B., P.B.R., N.J.F.); Department of Pathology, Duke University Medical Center, Durham, NC (R.C.B.); and MRC Centre for Developmental Neurobiology, King's College, London, UK (P.R.G.-W.).
Igor NepliouevFrom the Department of Medicine, Duke University Medical Center, Durham, NC (J.A.S., J.-H.W., L.Z., I.N., Z.-S.Z., V.G.B., L.B., P.B.R., N.J.F.); Department of Pathology, Duke University Medical Center, Durham, NC (R.C.B.); and MRC Centre for Developmental Neurobiology, King's College, London, UK (P.R.G.-W.).
Zhu-Shan ZhangFrom the Department of Medicine, Duke University Medical Center, Durham, NC (J.A.S., J.-H.W., L.Z., I.N., Z.-S.Z., V.G.B., L.B., P.B.R., N.J.F.); Department of Pathology, Duke University Medical Center, Durham, NC (R.C.B.); and MRC Centre for Developmental Neurobiology, King's College, London, UK (P.R.G.-W.).
Victoria G BrysonFrom the Department of Medicine, Duke University Medical Center, Durham, NC (J.A.S., J.-H.W., L.Z., I.N., Z.-S.Z., V.G.B., L.B., P.B.R., N.J.F.); Department of Pathology, Duke University Medical Center, Durham, NC (R.C.B.); and MRC Centre for Developmental Neurobiology, King's College, London, UK (P.R.G.-W.).
Leigh BrianFrom the Department of Medicine, Duke University Medical Center, Durham, NC (J.A.S., J.-H.W., L.Z., I.N., Z.-S.Z., V.G.B., L.B., P.B.R., N.J.F.); Department of Pathology, Duke University Medical Center, Durham, NC (R.C.B.); and MRC Centre for Developmental Neurobiology, King's College, London, UK (P.R.G.-W.).
Rex C BentleyFrom the Department of Medicine, Duke University Medical Center, Durham, NC (J.A.S., J.-H.W., L.Z., I.N., Z.-S.Z., V.G.B., L.B., P.B.R., N.J.F.); Department of Pathology, Duke University Medical Center, Durham, NC (R.C.B.); and MRC Centre for Developmental Neurobiology, King's College, London, UK (P.R.G.-W.).
Phillip R Gordon-WeeksFrom the Department of Medicine, Duke University Medical Center, Durham, NC (J.A.S., J.-H.W., L.Z., I.N., Z.-S.Z., V.G.B., L.B., P.B.R., N.J.F.); Department of Pathology, Duke University Medical Center, Durham, NC (R.C.B.); and MRC Centre for Developmental Neurobiology, King's College, London, UK (P.R.G.-W.).
Paul B RosenbergFrom the Department of Medicine, Duke University Medical Center, Durham, NC (J.A.S., J.-H.W., L.Z., I.N., Z.-S.Z., V.G.B., L.B., P.B.R., N.J.F.); Department of Pathology, Duke University Medical Center, Durham, NC (R.C.B.); and MRC Centre for Developmental Neurobiology, King's College, London, UK (P.R.G.-W.).
Neil J FreedmanFrom the Department of Medicine, Duke University Medical Center, Durham, NC (J.A.S., J.-H.W., L.Z., I.N., Z.-S.Z., V.G.B., L.B., P.B.R., N.J.F.); Department of Pathology, Duke University Medical Center, Durham, NC (R.C.B.); and MRC Centre for Developmental Neurobiology, King's College, London, UK (P.R.G.-W.).
Duke University Hospital · USDuke Medical Center · US

Funding

Resource Core 3 - Metabolomics CoreP30AG028716 · NIA · DUKE UNIVERSITY · PI Virginia B Kraus · 2006 to 2026
$24.6M
MULTIDISCIPLINARY HEART &VASCULAR DISEASEST32HL007101 · NHLBI · DUKE UNIVERSITY · PI FREEDMAN, NEIL J. · 1985 to 2020
$9.8M
Renal Genomics CoreP30DK096493 · NIDDK · DUKE UNIVERSITY · PI COFFMAN, THOMAS M · 2012 to 2016
$5.9M
Role of Drebrin in Vascular Smooth Muscle RemodelingR01HL112901 · NHLBI · DUKE UNIVERSITY · PI STIBER, JONATHAN A · 2013 to 2017
$1.9M
Anti-atherogenic Mechanisms of the Dual Rho-GEF KalirinR01HL121689 · NHLBI · DUKE UNIVERSITY · PI FREEDMAN, NEIL J. · 2014 to 2017
$1.9M
Role of Drebrin in AtherosclerosisR01HL121531 · NHLBI · DUKE UNIVERSITY · PI STIBER, JONATHAN A · 2014 to 2017
$1.1M
NHLBI NIH HHS R01 HL112901NHLBI NIH HHS R01 HL121531NHLBI NIH HHS R01 HL121689NHLBI NIH HHS T32 HL007101NIA NIH HHS P30 AG028716NIDDK NIH HHS P30 DK096493
6 · The paper itself

Abstract

objectiveVascular smooth muscle cell (SMC) migration is regulated by cytoskeletal remodeling as well as by certain transient receptor potential (TRP) channels, nonselective cation channels that modulate calcium influx. Proper function of multiple subfamily C TRP (TRPC) channels requires the scaffolding protein Homer 1, which associates with the actin-binding protein Drebrin. We found that SMC Drebrin expression is upregulated in atherosclerosis and in response to injury and investigated whether Drebrin inhibits SMC activation, either through regulation of TRP channel function via Homer or through a direct effect on the actin cytoskeleton. APPROACH AND

resultsWild-type (WT) and congenic Dbn(-/+) mice were subjected to wire-mediated carotid endothelial denudation. Subsequent neointimal hyperplasia was 2.4±0.3-fold greater in Dbn(-/+) than in WT mice. Levels of globular actin were equivalent in Dbn(-/+) and WT SMCs, but there was a 2.4±0.5-fold decrease in filamentous actin in Dbn(-/+) SMCs compared with WT. Filamentous actin was restored to WT levels in Dbn(-/+) SMCs by adenoviral-mediated rescue expression of Drebrin. Compared with WT SMCs, Dbn(-/+) SMCs exhibited increased TRP channel activity in response to platelet-derived growth factor, increased migration assessed in Boyden chambers, and increased proliferation. Enhanced TRP channel activity and migration in Dbn(-/+) SMCs were normalized to WT levels by rescue expression of not only WT Drebrin but also a mutant Drebrin isoform that binds actin but fails to bind Homer.

conclusionsDrebrin reduces SMC activation through its interaction with the actin cytoskeleton but independently of its interaction with Homer scaffolds.

Indexed as

NeointimaActin CytoskeletonActinsAnimalsAtherosclerosisCarotid ArteriesCarotid Artery InjuriesCell MovementCell ProliferationCells, CulturedDisease Models, AnimalGenotypeHomer Scaffolding ProteinsHumansHyperplasiaMice, Inbred C57BLActinsdrebrinsHomer Scaffolding ProteinsNeuropeptidesTransient Receptor Potential ChannelsactinDrebrinhomerneointimal hyperplasiasmooth muscle

Identifiers

PMID27013612
PMCPMC4850108
OpenAlexW2312061967

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.