Evidence map›Paper›PMID 20018948›Full record

ArticleAmerican journal of physiology. Cell physiology2010

Actin polymerization in differentiated vascular smooth muscle cells requires vasodilator-stimulated phosphoprotein.

Hak Rim Kim, Philip Graceffa, François Ferron, Cynthia Gallant, Malgorzata Boczkowska, Roberto Dominguez, Kathleen G Morgan

Abstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

44 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
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  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Acetylation of Abelson interactor 1 at K416 regulates actin cytoskeleton and smooth muscle contraction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. VASP Regulates NK Cell Lytic Granule Convergence.Journal of immunology (Baltimore, Md. : 1950) · 2018
    Article
  15. Article
  16. Article
  17. Actin polymerization contributes to enhanced pulmonary vasoconstrictor reactivity after chronic hypoxia.American journal of physiology. Heart and circulatory physiology · 2018
    Article
  18. Article
  19. Article
  20. Review
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

7 authors at 3 institutions in 1 country.

Hak Rim KimDept. of Health Sciences, Boston Univ., 635 Commonwealth Ave, Boston MA 02215, USA.
Philip Graceffa
François Ferron
Cynthia Gallant
Malgorzata Boczkowska
Roberto Dominguez
Kathleen G Morgan
University of Pennsylvania · USBoston Biomedical Research Institute · USBoston University · US

Funding

Structure-Function of the CytoskeletonP01HL086655 · NHLBI · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI MORGAN, KATHLEEN G · 2007 to 2011
$8.8M
NHLBI NIH HHS P01 HL086655NHLBI NIH HHS P01 HL-86655
6 · The paper itself

Abstract

Our group has previously shown that vasoconstrictors increase net actin polymerization in differentiated vascular smooth muscle cells (dVSMC) and that increased actin polymerization is linked to contractility of vascular tissue (Kim et al., Am J Physiol Cell Physiol 295: C768-778, 2008). However, the underlying mechanisms are largely unknown. Here, we evaluated the possible functions of the Ena/vasodilator-stimulated phosphoprotein (VASP) family of actin filament elongation factors in dVSMC. Inhibition of actin filament elongation by cytochalasin D decreases contractility without changing myosin light-chain phosphorylation levels, suggesting that actin filament elongation is necessary for dVSM contraction. VASP is the only Ena/VASP protein highly expressed in aorta tissues, and VASP knockdown decreased smooth muscle contractility. VASP partially colocalizes with alpha-actinin and vinculin in dVSMC. Profilin, known to associate with G actin and VASP, also colocalizes with alpha-actinin and vinculin, potentially identifying the dense bodies and the adhesion plaques as hot spots of actin polymerization. The EVH1 domain of Ena/VASP is known to target these proteins to their sites of action. Introduction of an expressed EVH1 domain as a dominant negative inhibits stimulus-induced increases in actin polymerization. VASP phosphorylation, known to inhibit actin polymerization, is decreased during phenylephrine stimulation in dVSMC. We also directly visualized, for the first time, rhodamine-labeled actin incorporation in dVSMC and identified hot spots of actin polymerization in the cell cortex that colocalize with VASP. These results indicate a role for VASP in actin filament assembly, specifically at the cell cortex, that modulates contractility in dVSMC.

Indexed as

Cell DifferentiationVasoconstrictionActininActinsAdrenergic alpha-AgonistsAmino Acid SequenceAnimalsAortaCell Adhesion MoleculesCytochalasin DFerretsHumansMicrofilament ProteinsMicroscopy, FluorescenceModels, MolecularMolecular Sequence DataActininActinsAdrenergic alpha-AgonistsCell Adhesion MoleculesCytochalasin DEVL protein, humanMicrofilament ProteinsOligonucleotides, AntisensePhenylephrinePhosphoproteinsProfilinsRecombinant Fusion ProteinsVasoconstrictor AgentsVasodilator-Stimulated PhosphoproteinVinculin

Identifiers

PMID20018948
PMCPMC2838578
OpenAlexW2085785974

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.