Atherosclerosis

2003

DOI: 10.1016/s0021-9150(03)00150-3

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Haptoglobin elutes from human atherosclerotic coronary arteries—a potential marker of arterial pathology

Maria A Matuszek

¹

,

Lina Panayiota Aristoteli

²

,

³

et al.

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Introduction2

Discussion1

Systemic Low Grade Inflammation1

New South Wales1

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Cited by 14 publications

(9 citation statements)

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“…Its production is induced by cytokines (van Vlierberghe et al 2004). There is a plausible role for Hp in vascular disease as both oxidative and inflammatory factors are important in the pathogenesis of atherosclerosis, and its presence has been shown in atherosclerotic coronary lesions (Ross 1999;Matuszek et al 2003). High levels of Hp have been associated with the Fig.…”

Section: Discussionmentioning

confidence: 99%

A SELDI-TOF-MS Study in Lacunar Stroke with Subsequent Haptoglobin Phenotyping

Bons²,

et al. 2008

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Using Surface-Enhanced Laser Desorption / Ionization Time-of-Flight Mass Spectrometry (SELDI-TOF-MS), we aimed to detect differences in protein profile in serum samples of two lacunar stroke subtypes. SELDI-TOF-MS, followed by protein identification, was performed in samples of 8 first-ever lacunar stroke patients with MR imaging showing a single symptomatic lacunar lesion (type 1), and 8 with multiple additional "silent" lacunar lesions and extensive white matter lesions (type 2). A 16 kDa protein, identified as alpha-2-chain of haptoglobin (Hp), was found to be overrepresented in type 1 compared to type 2 (peak intensity 12.5 vs. 5.0; p=0.02). As a polymorphism with two alleles, Hp-1 and Hp 2, determines the presence of alpha-1 and/or alpha-2-chains in the Hp-molecule, Hp phenotypic analysis was performed. Hp 1 : Hp-2 allele frequency was 0.562 : 0.438 in type 1 and 0.812 : 0.188 in type 2 (population reference approximately 0.4 : 0.6). We conclude that the overrepresentation of the alpha-2-chain in lacunar stroke type 1 compared to type 2 relates to a higher Hp-2 allele frequency in the former. Yet, compared to population reference, the phenotype distribution in both patient groups deviates towards a high Hp-1 allele frequency. Our findings suggest a role for the Hp gene in the etiology of cerebral small vessel disease. Larger studies are now needed to explore this new candidate gene.

“…Its production is induced by cytokines (van Vlierberghe et al 2004). There is a plausible role for Hp in vascular disease as both oxidative and inflammatory factors are important in the pathogenesis of atherosclerosis, and its presence has been shown in atherosclerotic coronary lesions (Ross 1999;Matuszek et al 2003). High levels of Hp have been associated with the Fig.…”

Section: Discussionmentioning

confidence: 99%

A SELDI-TOF-MS Study in Lacunar Stroke with Subsequent Haptoglobin Phenotyping

Bons²,

et al. 2008

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Using Surface-Enhanced Laser Desorption / Ionization Time-of-Flight Mass Spectrometry (SELDI-TOF-MS), we aimed to detect differences in protein profile in serum samples of two lacunar stroke subtypes. SELDI-TOF-MS, followed by protein identification, was performed in samples of 8 first-ever lacunar stroke patients with MR imaging showing a single symptomatic lacunar lesion (type 1), and 8 with multiple additional "silent" lacunar lesions and extensive white matter lesions (type 2). A 16 kDa protein, identified as alpha-2-chain of haptoglobin (Hp), was found to be overrepresented in type 1 compared to type 2 (peak intensity 12.5 vs. 5.0; p=0.02). As a polymorphism with two alleles, Hp-1 and Hp 2, determines the presence of alpha-1 and/or alpha-2-chains in the Hp-molecule, Hp phenotypic analysis was performed. Hp 1 : Hp-2 allele frequency was 0.562 : 0.438 in type 1 and 0.812 : 0.188 in type 2 (population reference approximately 0.4 : 0.6). We conclude that the overrepresentation of the alpha-2-chain in lacunar stroke type 1 compared to type 2 relates to a higher Hp-2 allele frequency in the former. Yet, compared to population reference, the phenotype distribution in both patient groups deviates towards a high Hp-1 allele frequency. Our findings suggest a role for the Hp gene in the etiology of cerebral small vessel disease. Larger studies are now needed to explore this new candidate gene.

“…55 Although the suitability of increased haptoglobin level as a systemic marker for atherosclerosis remains to be established, eluting haptoglobin from atherosclerotic lesions in the arterial wall could distinguish between arteries with minor or extensive atherosclerosis. 56…”

Section: Systemic Low Grade Inflammationmentioning

confidence: 99%

Oxidative stress and systemic inflammation in patients with sleep apnea: Role of obesity

¹

,

²

,

³

2007

Sleep and Biological Rhythms

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Oxidative stress and systemic inflammation resulting from repeated hypoxia/reoxygenation cycles in obstructive sleep apnea-hypopnea syndrome (OSAHS) play a role in atherogenesis. It is unclear, however, if this association is independent of obesity. The aims of the present study were to compare markers of oxidative stress and systemic inflammation between patients with and without OSAHS independent of obesity, and to examine their interrelations. In experiment 1, 20 OSAHS patients, age 42.1 ± 10.0 years, body mass index 26.3 ± 2.7 kg/m 2 , and apnea-hypopnea index 28.8 ± 10.8 events/h, were individually matched with 20 control subjects, age 41.5 ± 11.1 years, body mass index 26.0 ± 2.9, and apnea-hypopnea index 6.5 ± 2.4 events/h. In experiment 2, 15 OSAHS patients with body mass index > 27 were individually matched with 15 OSAHS patients having the same age and similar apnea severity with body mass index < 27. In both experiments, blood was drawn at the end of the sleep study for determination of lipid peroxidation markers, thiobarbituric-acid-reactive substances (TBARS) and peroxides and the antioxidant enzyme paraoxonase-1, and the systemic inflammatory markers C-reactive protein (CRP), ceruloplasmin and haptoglobin. OSAHS patients had significantly higher concentrations of TBARS (P < 0.0002) and peroxides (P < 0.03) and lower paraoxonase-1 (P < 0.02) than controls. No differences were found for the inflammatory markers but only in OSAHS patients there were significant correlations between the lipid peroxidation and inflammatory markers. There were no differences in lipid peroxidation between obese and non-obese patients, but CRP was higher (P < 0.03) in the obese patients. We conclude that sleep apnea is primarily associated with increased oxidative stress. Possibly, OSAHS influences systemic inflammatory pathways indirectly through oxidative stress.

“…Using samples obtained from patients undergoing bypass surgery and coronary angiography, they found that coronary arteries release a number of molecules into the blood stream. One of these is haptoglobin, a protein not normally measured in patients with atherosclerosis, 72 but which is present at elevated levels in the circulation in patients with advanced coronary disease. This non‐invasive test has the potential to identify the presence of vulnerable atherosclerotic plaques before their rupture.…”

Section: New South Walesmentioning

confidence: 99%

Bench‐to‐bedside research in Australian research institutes: a snapshot

¹

2003

Medical Journal of Australia

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