Evidence map›Paper›PMID 21722586›Full record

ArticleJournal of diabetes science and technology2011

Glycated albumin modulates endothelial cell thrombogenic and inflammatory responses.

David A Rubenstein, Zahra Maria, Wei Yin

Open access · bronzeAbstract read
In one paragraph

Article in Journal of diabetes science and technology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.3field-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

21 citing papers in PubMed, 45 citations in OpenAlex.

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  9. Integrative Role of Albumin: Evolutionary, Biochemical and Pathophysiological Aspects.Journal of evolutionary biochemistry and physiology · 2021
    Article
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  12. Glycated albumin (GA) and inflammation: role of GA as a potential marker of inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018
    Review
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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

3 authors at 1 institution in 1 country.

David A RubensteinSchool of Mechanical and Aerospace Engineering, Oklahoma State University, Stillwater, Oklahoma, USA. david.rubenstein@okstate.edu
Zahra Maria
Wei Yin
Oklahoma State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIt has become established that a diabetic vasculature promotes cardiovascular disease progression via changes to endothelial cells, platelets, and the interactions of these cells. It is believed that the majority of these changes are induced by the presence of advanced glycation end products (AGEs), which permanently alter various functions. Studies have shown that platelets perpetuate endothelial cell responses under these conditions. However, the role of changes in endothelial cell thrombogenicity and inflammatory responses, after subjected to AGEs, has not been characterized. Our objective was to evaluate the effects of AGEs on these functions.

methodsTo accomplish this, albumin was chemically modified by exposure to glucose for up to 8 weeks, and endothelial cells were subjected to glycated albumin for up to 5 days in a cell culture system. A time course for changes in endothelial cell viability, density, morphology, and metabolic activity were investigated, along with the surface expression of intercellular adhesion molecule-1, thrombomodulin, tissue factor, connexin-43, and caveolin-1.

resultsEndothelial cells exposed to irreversibly glycated albumin were less viable, proliferated slower, and had a lower metabolic activity as compared to cells exposed to nonglycated albumin. Endothelial cells that were exposed to any glycated albumin were procoagulant and proinflammatory as compared with all other conditions. There were no overall trends in the expression of connexin-43 or caveolin-1.

conclusionsOur data suggest that the presence of irreversible glycated albumin is deleterious to endothelial cells, makes endothelial cells more procoagulant, and promotes inflammatory responses. It is therefore possible that endothelial cell activation may precede and promote platelet activation during diabetic conditions.

Indexed as

AlbuminsAnimalsBlood GlucoseCardiovascular DiseasesCattleCaveolin 1Connexin 43Diabetes ComplicationsDisease ProgressionEndothelial CellsGlycated Serum AlbuminGlycation End Products, AdvancedHumansHuman Umbilical Vein Endothelial CellsInflammationIntercellular Adhesion Molecule-1AlbuminsBlood GlucoseCaveolin 1Connexin 43Glycated Serum AlbuminGlycation End Products, AdvancedIntercellular Adhesion Molecule-1Serum AlbuminThrombinThrombogenThrombomodulin

Identifiers

PMID21722586
PMCPMC3192637
OpenAlexW2141770297

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.