Evidence map›Paper›PMID 25063792›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2014

Poldip2 controls vascular smooth muscle cell migration by regulating focal adhesion turnover and force polarization.

Srinivasa Raju Datla, Daniel J McGrail, Sasa Vukelic, Lauren P Huff, Alicia N Lyle, Lily Pounkova, Minyoung Lee, Bonnie Seidel-Rogol, Mazen K Khalil, Lula L Hilenski and 4 more

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 62 citations in OpenAlex.

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  15. Oxidative Stress and Hypertension.Circulation research · 2021
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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

14 authors at 3 institutions in 1 country.

Srinivasa Raju DatlaDepartment of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta;
Daniel J McGrailDepartment of Chemical and Biomolecular Engineering and.
Sasa VukelicDepartment of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta;
Lauren P HuffDepartment of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta;
Alicia N LyleDepartment of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta;
Lily PounkovaDepartment of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta;
Minyoung LeeDepartment of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta;
Bonnie Seidel-RogolDepartment of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta;
Mazen K KhalilDepartment of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta;
Lula L HilenskiDepartment of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta;
Lance S TeradaDepartment of Internal Medicine, Division of Pulmonary and Critical Care, University of Texas Southwestern Medical Center, Dallas, Texas.
Michelle R DawsonDepartment of Chemical and Biomolecular Engineering and The Petit Institute for Bioengineering and Bioscience, Georgia Institute of Technology, Atlanta, Georgia;
Bernard LassègueDepartment of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta;
Kathy K GriendlingDepartment of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta; kgriend@emory.edu.
Emory University · USGeorgia Institute of Technology · USThe University of Texas Southwestern Medical Center · US

Funding

Vascular Oxidases in MigrationR01HL058863 · NHLBI · EMORY UNIVERSITY · PI GRIENDLING, KATHY K · 1997 to 2014
$4.1M
NOX4 and vascular smooth muscle differentiationR37HL038206 · NHLBI · EMORY UNIVERSITY · PI GRIENDLING, KATHY K · 2006 to 2015
$3.8M
VASCULAR SMOOTH MUSCLE PHOSPHOLIPASE DR01HL038206 · NHLBI · EMORY UNIVERSITY · PI GRIENDLING, KATHY K · 1993 to 2005
$2.1M
DIACYLGLYCEROL SIGNALING IN VASCULAR SMOOTH MUSCLER29HL038206 · NHLBI · EMORY UNIVERSITY · PI GRIENDLING, KATHY K · 1987 to 1991
–
NHLBI NIH HHS HL058863NHLBI NIH HHS HL092120NHLBI NIH HHS HL38206NHLBI NIH HHS R01 HL058863NHLBI NIH HHS R37 HL038206
6 · The paper itself

Abstract

Polymerase-δ-interacting protein 2 (Poldip2) interacts with NADPH oxidase 4 (Nox4) and regulates migration; however, the precise underlying mechanisms are unclear. Here, we investigated the role of Poldip2 in focal adhesion turnover, as well as traction force generation and polarization. Poldip2 overexpression (AdPoldip2) in vascular smooth muscle cells (VSMCs) impairs PDGF-induced migration and induces a characteristic phenotype of long cytoplasmic extensions. AdPoldip2 also prevents the decrease in spreading and increased aspect ratio observed in response to PDGF and slightly impairs cell contraction. Moreover, AdPoldip2 blocks focal adhesion dissolution and sustains H2O2 levels in focal adhesions, whereas Poldip2 knockdown (siPoldip2) significantly decreases the number of focal adhesions. RhoA activity is unchanged when focal adhesion dissolution is stimulated in control cells but increases in AdPoldip2-treated cells. Inhibition of RhoA blocks Poldip2-mediated attenuation of focal adhesion dissolution, and overexpression of RhoA or focal adhesion kinase (FAK) reverses the loss of focal adhesions induced by siPoldip2, indicating that RhoA and FAK mediate the effect of Poldip2 on focal adhesions. Nox4 silencing prevents focal adhesion stabilization by AdPoldip2 and induces a phenotype similar to siPoldip2, suggesting a role for Nox4 in Poldip2-induced focal adhesion stability. As a consequence of impaired focal adhesion turnover, PDGF-treated AdPoldip2 cells are unable to reduce and polarize traction forces, a necessary first step in migration. These results implicate Poldip2 in VSMC migration via regulation of focal adhesion turnover and traction force generation in a Nox4/RhoA/FAK-dependent manner.

Indexed as

Cell MovementAnimalsCarrier ProteinsCell AdhesionCell PolarityFocal Adhesion Protein-Tyrosine KinasesFocal AdhesionsHydrogen PeroxideMuscle, Smooth, VascularMyocytes, Smooth MuscleNADPH Oxidase 4NADPH OxidasesPlatelet-Derived Growth FactorRatsrhoA GTP-Binding ProteinCarrier ProteinsFocal Adhesion Protein-Tyrosine KinasesHydrogen PeroxideNADPH Oxidase 4NADPH OxidasesNox4 protein, ratPlatelet-Derived Growth FactorPoldip2 protein, ratrhoA GTP-Binding Proteincytoskeletonfocal adhesionsNADPH oxidase 4polymerase-δ-interacting protein 2reactive oxygen speciestraction forcesvascular smooth muscle cells

Identifiers

PMID25063792
PMCPMC4187069
OpenAlexW2161585597

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.