Evidence map›Paper›PMID 28362840›Full record

ArticlePloS one2017

Aspirin-triggered resolvin D1 attenuates PDGF-induced vascular smooth muscle cell migration via the cyclic adenosine monophosphate/protein kinase A (cAMP/PKA) pathway.

Giorgio Mottola, Anuran Chatterjee, Bian Wu, Mian Chen, Michael S Conte

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 39 citations in OpenAlex.

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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.

Giorgio MottolaDepartment of Surgery, Division of Vascular and Endovascular Surgery, Cardiovascular Research Institute, University of California San Francisco, San Francisco, California, United States of America.ORCID http://orcid.org/0000-0003-0670-8619
Anuran ChatterjeeDepartment of Surgery, Division of Vascular and Endovascular Surgery, Cardiovascular Research Institute, University of California San Francisco, San Francisco, California, United States of America.
Bian WuDepartment of Surgery, Division of Vascular and Endovascular Surgery, Cardiovascular Research Institute, University of California San Francisco, San Francisco, California, United States of America.
Mian ChenDepartment of Surgery, Division of Vascular and Endovascular Surgery, Cardiovascular Research Institute, University of California San Francisco, San Francisco, California, United States of America.
Michael S ConteDepartment of Surgery, Division of Vascular and Endovascular Surgery, Cardiovascular Research Institute, University of California San Francisco, San Francisco, California, United States of America.
University of California, San Francisco · US

Funding

Specialized lipid mediators and mechanisms of resolution in vascular injuryR01HL119508 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CONTE, MICHAEL S · 2013 to 2016
$1.5M
NHLBI NIH HHS R01 HL119508
6 · The paper itself

Abstract

BACKGROUND AND

objectivesResolvin D1 (RvD1) is a specialized pro-resolving lipid mediator that has been previously shown to attenuate vascular smooth muscle cell (VSMC) migration, a key process in the development of intimal hyperplasia. We sought to investigate the role of the cAMP/PKA pathway in mediating the effects of the aspirin-triggered epimer 17R-RvD1 (AT-RvD1) on VSMC migration.

methodsVSMCs were harvested from human saphenous veins. VSMCs were analyzed for intracellular cAMP levels and PKA activity after exposure to AT-RvD1. Platelet-derived growth factor (PDGF)-induced migration and cytoskeletal changes in VSMCs were observed through scratch, Transwell, and cell shape assays in the presence or absence of a PKA inhibitor (Rp-8-Br-cAMP). Further investigation of the pathways involved in AT-RvD1 signaling was performed by measuring Rac1 activity, vasodilator stimulated phosphoprotein (VASP) phosphorylation and paxillin translocation. Finally, we examined the role of RvD1 receptors (GPR32 and ALX/FPR2) in AT-RvD1 induced effects on VSMC migration and PKA activity.

resultsTreatment with AT-RvD1 induced a significant increase in cAMP levels and PKA activity in VSMCs at 5 minutes and 30 minutes, respectively. AT-RvD1 attenuated PDGF-induced VSMC migration and cytoskeletal rearrangements. These effects were attenuated by the PKA inhibitor Rp-8-Br-cAMP, suggesting cAMP/PKA involvement. Treatment of VSMC with AT-RvD1 inhibited PDGF-stimulated Rac1 activity, increased VASP phosphorylation, and attenuated paxillin localization to focal adhesions; these effects were negated by the addition of Rp-8-Br-cAMP. The effects of AT-RvD1 on VSMC migration and PKA activity were attenuated by blocking ALX/FPR2, suggesting an important role of this G-protein coupled receptor.

conclusionsOur results suggest that AT-RvD1 attenuates PDGF-induced VSMC migration via ALX/FPR2 and cAMP/PKA. Interference with Rac1, VASP and paxillin function appear to mediate the downstream effects of AT-RvD1 on VSMC migration.

Indexed as

AspirinBlotting, WesternCell MovementCells, CulturedCyclic AMPCyclic AMP-Dependent Protein KinasesDocosahexaenoic AcidsHumansMuscle, Smooth, VascularMyocytes, Smooth MusclePhosphorylationPlatelet-Derived Growth Factorrac1 GTP-Binding ProteinSignal TransductionAspirinCyclic AMPCyclic AMP-Dependent Protein KinasesDocosahexaenoic AcidsPlatelet-Derived Growth Factorrac1 GTP-Binding Proteinresolvin D1

Identifiers

PMID28362840
PMCPMC5376330
OpenAlexW2601871883

What OpenQuestion holds

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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.