Evidence map›Paper›PMID 7980430›Full record

ArticleThe Biochemical journal1994

Characterization of proteoglycans associated with mouse splenic AA amyloidosis.

T Stenstad, J H Magnus, G Husby

Open access · greenAbstract readComparative Study
In one paragraph

Article in The Biochemical journal, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 41% 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

5 citing papers in PubMed, 33 citations in OpenAlex.

  1. The pattern recognition reagents RAGE VC1 and peptide p5 share common binding sites and exhibit specific reactivity with AA amyloid in mice.Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis · 2016
    Article
  2. Article
  3. Review of eprodisate for the treatment of renal disease in AA amyloidosis.International journal of nephrology and renovascular disease · 2012
    Article
  4. Development and evaluation of agents for targeting visceral amyloid.Tijdschrift voor nu[c]leaire geneeskunde · 2011
    Article
  5. In vivo molecular imaging of peripheral amyloidosis using heparin-binding peptides.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
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

3 authors at 2 institutions in 1 country.

T StenstadDepartment of Rheumatology, University of Tromsø, Norway.
J H Magnus
G Husby
Oslo University Hospital · NOUiT The Arctic University of Norway · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We here report for the first time on the chemical characteristics of proteoglycans associated with mouse splenic reactive AA amyloid. Amyloid was induced in CBA/J mice by two different procedures; conventional casein treatment and by employing Freund's complete adjuvant, accelerated by Trypan Blue. Pulse-labelling was employed at distinct stages during amyloid development, followed by [35S]proteoglycan characterization of organ extracts. Repetitive 35S injections were also administered during the phase where amyloid deposition occurred most rapidly. Proteoglycans were extracted with guanidine in the presence of protease inhibitors and purified. The results showed that the production of proteoglycans is dramatically enhanced during amyloidogenesis, the glycosaminoglycan and proteoglycan accumulation being not only dependent on alterations in proteoglycan catabolism, but rather on increased synthesis. The increment could be demonstrated even at the stage before microscopic detection of amyloid deposits, clearly suggesting that the upregulation of proteoglycan expression precedes amyloid fibril formation. Two major proteoglycans were found to accumulate in advanced splenic amyloid; one a heparan sulphate proteoglycan of approx. 200 kDa with a core protein of 70 kDa, the other a chondroitin sulphate proteoglycan of smaller size. Moreover, free dermatan sulphate chains seemed to specifically accumulate in the organs during amyloid fibrillogenesis. We suggest that free glycosaminoglycans may be a specific feature of amyloidosis and that different proteoglycans and glycosaminoglycans play a role in formation and stabilization of amyloid fibrils in vivo.

Indexed as

AmyloidosisAnimalsBlotting, WesternCaseinsChromatography, GelChromatography, Ion ExchangeDrug SynergismElectrophoresis, Polyacrylamide GelFemaleFreund's AdjuvantGlycosaminoglycansImmunohistochemistryMiceMice, Inbred CBAMicroscopy, ElectronMolecular WeightCaseinsFreund's AdjuvantGlycosaminoglycansProteoglycansSerum Amyloid A ProteinTrypan Blue

Identifiers

PMID7980430
PMCPMC1137378
OpenAlexW8860048

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.