Evidence map›Paper›PMID 29494632›Full record

ArticlePloS one2018

The effect of increasing the sulfation level of chondroitin sulfate on anticoagulant specific activity and activation of the kinin system.

J Hogwood, A Naggi, G Torri, C Page, P Rigsby, B Mulloy, E Gray

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 27 citations in OpenAlex.

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  11. Galactosaminoglycans: Medical Applications and Drawbacks.Molecules (Basel, Switzerland) · 2019
    Review
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  13. 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 2 countries.

J HogwoodNational Institute for Biological Standards and Control, Blanche Lane, Herts, United Kingdom.ORCID 0000-0002-2595-1510
A NaggiInstitute for Chemical and Biochemical Research ''G. Ronzoni", Milan, Italy.
G TorriInstitute for Chemical and Biochemical Research ''G. Ronzoni", Milan, Italy.
C PageSacker Institute of Pulmonary Pharmacology, Institute of Pharmaceutical Science, King's College London, United Kingdom.
P RigsbyNational Institute for Biological Standards and Control, Blanche Lane, Herts, United Kingdom.
B MulloySacker Institute of Pulmonary Pharmacology, Institute of Pharmaceutical Science, King's College London, United Kingdom.
E GrayNational Institute for Biological Standards and Control, Blanche Lane, Herts, United Kingdom.
King's College London · GBIstituto di Ricerche Chimiche e Biochimiche G. Ronzoni · ITNational Institute for Biological Standards and Control · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oversulfated chondroitin sulfate (OSCS) was identified as a contaminant in certain heparin preparations as the cause of adverse reactions in patients. OSCS was found to possess both plasma anticoagulant activity and the ability to activate prekallikrein to kallikrein. Differentially sulfated chondroitin sulfates were prepared by synthetic modification of chondroitin sulfate and were compared to the activity of OSCS purified from contaminated heparin. Whilst chondroitin sulfate was found to have minimal anticoagulant activity, increasing sulfation levels produced an anticoagulant response which we directly show for the first time is mediated through heparin cofactor II. However, the tetra-sulfated preparations did not possess any higher anticoagulant activity than several tri-sulfated variants, and also had lower heparin cofactor II mediated activity. Activation of prekallikrein was concentration dependent for all samples, and broadly increased with the degree of sulfation, though the di-sulfated preparation was able to form more kallikrein than some of the tri-sulfated preparations. The ability of the samples to activate the kinin system, as measured by bradykinin, was observed to be through kallikrein generation. These results show that whilst an increase in sulfation of chondroitin sulfate did cause an increase in anticoagulant activity and activation of the kinin system, there may be subtler structural interactions other than sulfation at play given the different responses observed.

Indexed as

AnimalsAnticoagulantsBradykininChondroitin SulfatesDose-Response Relationship, DrugDrug ContaminationEnzyme ActivationHeparinHeparin Cofactor IIHumansKallikreinsStructure-Activity RelationshipAnticoagulantsBradykininChondroitin SulfatesHeparinHeparin Cofactor IIKallikreins

Identifiers

PMID29494632
PMCPMC5832253
OpenAlexW2793742498

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.