Marked decrease in the levels of two inflammatory markers, hs-C-reactive protein and fibrinogen in patients with severe carotid atherosclerosis after eversion carotid endarterectomy

Dósa, Edit; Rugonfalvi-Kiss, Szabolcs; Prohászka, Zoltán; Szabó, Attila; Karádi, István; Selmeci, L.; Romics, L; Füst, G.; Acsády, György; Entz, László

doi:10.1007/s00011-004-1304-y

Cited by 20 publications

(29 citation statements)

References 21 publications

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“…Patients included in the present study represent a subgroup of a prospective study of 123 consecutive patients, in which MBL2 genotypes, 9 changes in CRP 16 and C3 10 levels were previously published. The reason for including less patients in the present study was the limited availability of the serum samples, otherwise the study setup was the same.…”

Section: Methodsmentioning

confidence: 99%

“…The reason for including less patients in the present study was the limited availability of the serum samples, otherwise the study setup was the same. 9,10,16 Briefly, all patients underwent eversion type CEA: the surgical technique has been described earlier. 17 The indication for CEA was in accordance with the American Heart Association guidelines.…”

Section: Methodsmentioning

confidence: 99%

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Low C1-Inhibitor Levels Predict Early Restenosis After Eversion Carotid Endarterectomy

Varga

Laki

Dósa

et al. 2007

ATVB

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Objective-Homozygotes for the normal (A) allele of mannose-binding lectin (MBL2) gene have higher risks to develop an early restenosis after eversion carotid endarterectomy (CEA). Activation of the lectin pathway is regulated by C1-inhibitor (C1-INH). The objective of the present study was to determine the predictive value of C1-INH in restenosis after CEA. Methods and Results-C1-INH and MBL-associated serine protease-2 (MASP-2) were determined in samples serially taken from 64 patients with CEA, who were followed-up with carotid duplex scan (CDS) examinations for 14 months. MBL2 genotypes were also determined.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Low C1-Inhibitor Levels Predict Early Restenosis After Eversion Carotid Endarterectomy

Varga

Laki

Dósa

et al. 2007

ATVB

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“…32 Nevertheless, the removal of atherosclerotic plaques from the carotid arteries markedly decreases the production of high sensibility-CRP and fibrinogen, probably because of the decrease in the inflammatory burden or the removal of the advanced plaques able to produce these proteins. 33 At present, there is not sufficient evidence to recommend measurement of CRP in the routine evaluation of cerebrovascular disease risk in primary prevention.…”

Section: Systemic Markers Of Atherosclerotic Inflammatory Processesmentioning

confidence: 99%

The Vulnerable Carotid Artery Plaque

Nighoghossian

Derex

Douek

2005

Stroke

214

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Background and Purpose-Atherosclerosis is a diffuse, chronic inflammatory disorder that involves the vascular, metabolic, and immune systems and leads to plaque vulnerability. The traditional risk assessment relies on clinical, biological, and conventional imaging tools. However, these tools fall short in predicting near-future events in patients with vulnerable carotid artery plaque. Methods-In current clinical practice, anatomic imaging modalities, such as B-mode ultrasound, spiral computed tomography angiography, and high-resolution MRI, can identify several morphological features characteristic of the vulnerable plaque but give little or no information regarding molecular and cellular mechanisms. Results-This review is dedicated to factors involved in carotid artery plaque vulnerability and to new imaging methods that target this condition. Our aim is to describe the following: (1) conventional pathologic and imaging markers predictive of plaque vulnerability; (2) the role of relevant biological, genetic, and mechanical factors; (3) the potential of new imaging methods; and (4) current and emerging treatments. Conclusions-A multimodal assessment of plaque vulnerability involving the combination of systemic markers, new imaging methods that target inflammatory and thrombotic components, and the potential of emerging therapies may lead to a new stratification system for atherothrombotic risk and to a better prevention of atherothrombotic stroke.

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“…The earlier studies showed that fibrinogen and its degradation products are involved in the development of atherosclerosis by mediating inflammatory responses and participating in thrombosis formation [15-19]. Fibrinopeptide A (FPA) is a peptide of 16 amino acids which occurs as a natural consequence of hemostasis from proteolysis of fibrinogen’s Aα chain [20].…”

Section: Introductionmentioning

confidence: 99%

Fibrinopeptide A Induces Expression of C-Reactive Protein via the ROS-ERK1/2/ P38-NF-κB Signal Pathway in Vascular Smooth Muscle Cells

Zhao

Liu

et al. 2018

Cell Physiol Biochem

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Background/Aims: Atherosclerosis is a chronic inflammatory disease in the artery walls. Fibrinopeptide A (FPA) is a biomarker of the activation of coagulation system, and a high concentration of FPA in blood occurs in patients with ischemic heart disease etc. However, there exist few studies on the pathological effects of FPA in cardiovascular system. Therefore, the present study examined the effect of FPA on CRP expression in VSMCs and the molecular mechanisms. Methods: mRNA and protein expression was identified by quantitative real-time PCR and Western blot, respectively. Reactive oxygen species (ROS) and the immunofluorescence staining were observed by a fluorescence microscope. Plasma FPA and CRP level was determined by ELISA. Results: FPA induced the expressions of CRP, IL-1β and IL-6 in VSMCs, and anti-IL-1β and anti-IL-6 neutralizing antibodies partially reduced FPA-induced CRP expression in VSMCs. The subchronic administration of FPA to rats increased FPA level in plasma and CRP expression in the aortic artery walls. The further studies showed that FPA promoted superoxide anion generation in VSMCs. Antioxidant NAC antagonized FPA-stimulated superoxide anion generation and inhibited FPA-induced CRP expression in VSMCs. FPA activated ERK1/2 and p38 phosphorylation, and PD98059 and SB203580 reduced FPA-induced CRP expression. Moreover, NAC inhibited the activation of ERK1/2 and p38. In addition, FPA enhanced NF-κB level in the nuclei of VSMCs, and PDTC reduced FPA-induced expression of CRP. Conclusions: FPA induces CRP expression in VSMCs via ROS-ERK1/2/p38-NF-κB signal pathway. This finding for the first time provides an experimental evidence for pro-inflammatory effect of FPA.

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Marked decrease in the levels of two inflammatory markers, hs-C-reactive protein and fibrinogen in patients with severe carotid atherosclerosis after eversion carotid endarterectomy

Abstract: Our present findings indicate that removal of atherosclerotic plaques from the carotid arteries markedly decreases the production of two acute phase proteins due to the decrease of the inflammatory burden or the removal of the advanced plaques able to produce these proteins.

Cited by 20 publications

References 21 publications

Low C1-Inhibitor Levels Predict Early Restenosis After Eversion Carotid Endarterectomy

Low C1-Inhibitor Levels Predict Early Restenosis After Eversion Carotid Endarterectomy

The Vulnerable Carotid Artery Plaque

Fibrinopeptide A Induces Expression of C-Reactive Protein via the ROS-ERK1/2/ P38-NF-κB Signal Pathway in Vascular Smooth Muscle Cells

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