Evidence map›Paper›PMID 12813008›Full record

ArticleBritish journal of pharmacology2003

Effects of heparin and related molecules upon neutrophil aggregation and elastase release in vitro.

Rachel A Brown, Rebecca Lever, Neil A Jones, Clive P Page

Open access · greenAbstract read
In one paragraph

Article in British journal of pharmacology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

22 citing papers in PubMed, 67 citations in OpenAlex.

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  9. Targeted donor complement blockade after brain death prevents delayed graft function in a nonhuman primate model of kidney transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2020
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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

4 authors at 1 institution in 1 country.

Rachel A BrownSackler Institute of Pulmonary Pharmacology, Guy's, King's and St Thomas' School of Biomedical Sciences, King's College London, London. rachael.2.brown@kcl.ac.uk
Rebecca Lever
Neil A Jones
Clive P Page
King's College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1 Neutrophil-derived elastase is an enzyme implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD). Heparin inhibits the enzymatic activity of elastase and here we provide evidence for the first time that heparin can inhibit the release of elastase from human neutrophils. 2 Unfractionated and low molecular weight heparins (UH and LMWH, 0.01-1000 U ml(-1)) and corresponding concentrations (0.06-6000 micro g ml(-1)) of nonanticoagulant O-desulphated heparin (ODH), dextran sulphate (DS) and nonsulphated poly-L-glutamic acid (PGA) were compared for their effects on both elastase release from and aggregation of neutrophils. 3 UH, ODH and LMWH inhibited (P<0.05) the homotypic aggregation of neutrophils, in response to both N-formyl-methionyl-leucyl-phenylalanine (fMLP, 10(-6) M) and platelet-activating factor (PAF, 10(-6) M), as well as elastase release in response to these stimuli, in the absence and presence of the priming agent tumour necrosis factor-alpha (TNF-alpha, 100 U ml(-1)). 4 DS inhibited elastase release under all the conditions of cellular activation tested (P<0.05) but had no effect on aggregation. PGA lacked efficacy in either assay, suggesting general sulphation to be important in both effects of heparin on neutrophil function and specific patterns of sulphation to be required for inhibition of aggregation. 5 Further investigation of the structural requirements for inhibition of elastase release confirmed the nonsulphated GAG hyaluronic acid and neutral dextran, respectively, to be without effect, whereas the IP(3) receptor antagonist 2-aminoethoxydiphenylborate (2-APB) mimicked the effects of heparin, itself an established IP(3) receptor antagonist, suggesting this to be a possible mechanism of action.

Indexed as

Boron CompoundsCell AggregationDextran SulfateHeparinHeparin, Low-Molecular-WeightHumansHyaluronic AcidLeukocyte ElastaseNeutrophilsN-Formylmethionine Leucyl-PhenylalaninePlatelet Activating FactorTumor Necrosis Factor-alpha2-aminoethoxydiphenyl borateBoron CompoundsDextran SulfateHeparinHeparin, Low-Molecular-WeightHyaluronic AcidLeukocyte ElastaseN-Formylmethionine Leucyl-PhenylalaninePlatelet Activating FactorTumor Necrosis Factor-alpha

Identifiers

PMID12813008
PMCPMC1573888
OpenAlexW1976320491

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.