Literature DB >> 15314081

More fibrosis and thrombotic complications but similar expression patterns of markers for coagulation and inflammation in symptomatic plaques from DM2 patients.

Dirkje W Sommeijer1, Aida Beganovic, Casper G Schalkwijk, Hanneke Ploegmakers, Chris M van der Loos, Benien E van Aken, Hugo ten Cate, Allard C van der Wal.   

Abstract

OBJECTIVE: One of the possible pathological mechanisms behind the increased vascular injury in diabetes mellitus type 2 (DM2) is the formation of advanced glycation end products (AGEs). The aim of this study was to investigate whether the presence of AGEs and specific markers for coagulation and inflammation in symptomatic atherosclerotic plaques from DM2 patients differs from plaques from nondiabetics. METHODS AND
RESULTS: Carotid atherectomies were obtained from DM2 patients (n=11) and controls without DM2 matched for age and other cardiovascular risk factors (n=12) who were treated for symptomatic carotid artery stenosis. Plaques were graded according to the American Heart Association classification of lesions. More fibrosis and more thrombotic complications (p=0.007) were observed in carotid atherectomies from DM2 patients. Percentages of immunostained smooth muscle cells and macrophages in the lesions, quantified planimetrically, did not differ between the two groups. No differences were found in the immunostaining for T cells, tissue factor (TF), endothelial protein C receptor (EPCR), nuclear factor kappaB, and the AGE carboxymethyllysine.
CONCLUSIONS: These findings demonstrate that DM2 is associated with increased plaque complications; however, a local changed presence of AGEs, TF, and EPCR seems not to be involved in this end stage of atherosclerosis. Copyright The Histochemical Society, Inc.

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Year:  2004        PMID: 15314081     DOI: 10.1369/jhc.3A6207.2004

Source DB:  PubMed          Journal:  J Histochem Cytochem        ISSN: 0022-1554            Impact factor:   2.479


  5 in total

1.  Glycated albumin modulates endothelial cell thrombogenic and inflammatory responses.

Authors:  David A Rubenstein; Zahra Maria; Wei Yin
Journal:  J Diabetes Sci Technol       Date:  2011-05-01

2.  Smooth muscle homeostasis in human atherosclerotic plaques through interleukin 15 signalling.

Authors:  Jelger J van der Meer; Onno J de Boer; Peter Teeling; Chris M van der Loos; Mark C Dessing; Allard C van der Wal
Journal:  Int J Clin Exp Pathol       Date:  2011-03-22

3.  Glycaemic status influences the nature and severity of coronary artery disease.

Authors:  C Berry; S Noble; J C Grégoire; R Ibrahim; S Levesquie; M-A Lavoie; P L L'Allier; J-C Tardif
Journal:  Diabetologia       Date:  2010-01-14       Impact factor: 10.122

4.  Low numbers of FOXP3 positive regulatory T cells are present in all developmental stages of human atherosclerotic lesions.

Authors:  Onno J de Boer; Jelger J van der Meer; Peter Teeling; Chris M van der Loos; Allard C van der Wal
Journal:  PLoS One       Date:  2007-08-22       Impact factor: 3.240

Review 5.  Pleiotropic actions of factor Xa inhibition in cardiovascular prevention: mechanistic insights and implications for anti-thrombotic treatment.

Authors:  Hugo Ten Cate; Tomasz J Guzik; John Eikelboom; Henri M H Spronk
Journal:  Cardiovasc Res       Date:  2021-07-27       Impact factor: 10.787

  5 in total

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