Evidence map›Paper›PMID 16179391›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2005

C-type natriuretic peptide inhibits leukocyte recruitment and platelet-leukocyte interactions via suppression of P-selectin expression.

Ramona S Scotland, Marc Cohen, Paul Foster, Matthew Lovell, Anthony Mathur, Amrita Ahluwalia, Adrian J Hobbs

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

Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.0field-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

39 citing papers in PubMed, 100 citations in OpenAlex.

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  11. C-type natriuretic peptide is a pivotal regulator of metabolic homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2022
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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

7 authors at 3 institutions in 1 country.

Ramona S ScotlandWolfson Institute for Biomedical Research, University College London, Cruciform Building, Gower Street, London WC1E 6AE, United Kingdom.
Marc Cohen
Paul Foster
Matthew Lovell
Anthony Mathur
Amrita Ahluwalia
Adrian J Hobbs
University College London · GBUniversity of London · GBWilliam Harvey Research Institute · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

The multifaceted process of immune cell recruitment to sites of tissue injury is key to the development of an inflammatory response and involved in the pathogenesis of numerous cardiovascular disorders. We recently identified C-type natriuretic peptide (CNP) as an important endothelium-derived mediator that regulates vascular tone and protects against myocardial ischemia/reperfusion injury. Herein, we investigated whether CNP inhibits leukocyte recruitment and platelet aggregation and thereby exerts a potential antiinflammatory influence on the blood vessel wall. We assessed the effects of CNP on leukocyte-endothelial cell interactions in mouse mesenteric postcapillary venules in vivo in animals with high basal leukocyte activation (endothelial nitric oxide synthase knockout mice, eNOS(-/-)) or under acute inflammatory conditions (induced by interleukin-1beta or histamine). CNP suppressed basal leukocyte rolling in eNOS(-/-) mice in a rapid, reversible, and concentration-dependent manner. These effects of CNP were mimicked by the selective natriuretic peptide receptor-C agonist cANF(4-23). CNP also suppressed leukocyte rolling induced by IL-1beta or histamine, inhibited platelet-leukocyte interactions, and prevented thrombin-induced platelet aggregation of human blood. Furthermore, analysis of human umbilical vein endothelial cells, leukocytes, and platelets revealed that CNP selectively attenuates expression of P-selectin. Thus, CNP is a modulator of acute inflammation in the blood vessel wall characterized by leukocyte and platelet activation. These antiinflammatory effects appear to be mediated, at least in part, via suppression of P-selectin expression. These observations suggest that endothelial CNP might maintain an anti-atherogenic influence on the blood vessel wall and represent a target for therapeutic intervention in inflammatory cardiovascular disorders.

Indexed as

Analysis of VarianceAnimalsAtrial Natriuretic FactorEndothelium, VascularFlow CytometryGene Expression RegulationHumansInflammationLeukocytesMiceMice, KnockoutNatriuretic Peptide, C-TypeNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIPeptide FragmentsPlatelet AggregationAtrial Natriuretic Factoratrial natriuretic factor (4-23)NH2, de-Gln(18)-de-Ser(19)-de-Gly(20,22)-de-Leu(21)-Natriuretic Peptide, C-TypeNitric Oxide Synthase Type IINitric Oxide Synthase Type IIINos3 protein, mousePeptide FragmentsP-Selectin

Identifiers

PMID16179391
PMCPMC1242301
OpenAlexW2084077120

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.