Evidence map›Paper›PMID 20705916›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2010

Nitric oxide synthase expression and functional response to nitric oxide are both important modulators of circulating angiogenic cell response to angiogenic stimuli.

Christian Heiss, Andrea Schanz, Nicolas Amabile, Sarah Jahn, Qiumei Chen, Maelene L Wong, Tienush Rassaf, Yvonne Heinen, Miriam Cortese-Krott, William Grossman and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2010. 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
2.2field-weighted citation impact, top 13% 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, 55 citations in OpenAlex.

  1. Role of Endothelial Progenitor Cells in Frailty.International journal of molecular sciences · 2023
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  12. Vascular Complications of Cancer Chemotherapy.The Canadian journal of cardiology · 2016
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  19. 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

12 authors at 1 institution in 1 country.

Christian HeissDivision of Cardiology, University of California, San Francisco, San Francisco, CA 94143-0124, USA.
Andrea Schanz
Nicolas Amabile
Sarah Jahn
Qiumei Chen
Maelene L Wong
Tienush Rassaf
Yvonne Heinen
Miriam Cortese-Krott
William Grossman
Yerem Yeghiazarians
Matthew L Springer
Heinrich Heine University Düsseldorf · DE

Funding

The Role of Nitric Oxide Synthase in Circulating Progenitor Cell FunctionR01HL086917 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SPRINGER, MATTHEW LAWRENCE · 2007 to 2011
$2.1M
NHLBI NIH HHS HL086917NHLBI NIH HHS R01 HL086917
6 · The paper itself

Abstract

objectiveCirculating angiogenic cells (CACs), also termed endothelial progenitor cells, play an integral role in vascular repair and are functionally impaired in coronary artery disease (CAD). The role of nitric oxide (NO) in CAC function is poorly understood. We hypothesized that CAC migration toward angiogenic signals is modulated by both NO synthase (NOS) expression and functional response to NO. METHODS AND

resultsSimilar to endothelial cells, CAC chemotaxis to vascular endothelial growth factor (VEGF) was blocked by inhibition of NOS, phosphatidylinositol 3-kinase, or guanylyl cyclase or by treatment with an NO scavenger. Addition of an NO donor (S-nitroso-N-acetylpenicillamine) and the NOS substrate l-arginine increased random cell migration (chemokinesis) and enhanced VEGF-dependent chemotaxis. Healthy CACs expressed endothelial NOS, but endothelial NOS was not detected in CAD patient CACs. Both chemokinesis and chemotaxis to VEGF of patient CACs were decreased compared with healthy CACs but were restored to healthy values by S-nitroso-N-acetylpenicillamine. In parallel, CAD patients exhibited lower flow-mediated vasodilation and plasma NO source nitrite than young, healthy subjects, indicating endothelial dysfunction with reduced NO bioavailability.

conclusionsNOS activity is required for CAC chemotaxis. In CAD patients, impairment of NOS expression and NO bioavailability, rather than response to NO, may contribute to dysfunction of CACs and limit their regenerative capacity.

Indexed as

Cell MovementChemotaxisEndothelial CellsHumansNeovascularization, PhysiologicNitric OxideNitric Oxide SynthaseStem CellsVascular Endothelial Growth Factor ANitric OxideNitric Oxide SynthaseVascular Endothelial Growth Factor A

Identifiers

PMID20705916
PMCPMC2959135
OpenAlexW2129865811

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.