Measurement of desmosine and isodesmosine by capillary zone electrophoresis

Giummelly, Philippe; Botton, Bernard; Friot, Raphaëlle; Putra, Deddi Prima; Atkinson, Jeffrey

doi:10.1016/0021-9673(95)00487-4

Cited by 22 publications

(17 citation statements)

References 12 publications

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“…It was decided to use CE in the micellar electrokinetic chromatographic modality since the previously reported free solution CE mode of separation (capillary zone electrophoresis) of DES and IDES from hydrolysed elastin did not give satisfactory resolution of the two peaks [19]. The addition of a micellar buffer modifier such as sodium dodecyl sulphate to the background electrolyte provided enhanced resolution, thus yielding almost complete separation of the two compounds [13].…”

Section: Discussionmentioning

confidence: 99%

MEKC of desmosine and isodesmosine in urine of chronic destructive lung disease patients

Viglio¹,

Iadarola²,

Lupi³

et al. 2000

Eur Respir J

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Degradation of extracellular matrix components is central to many pathological features of chronic destructive lung disorders. Desmosine and isodesmosine are elastin-derived cross-linked amino acids whose urine levels are considered representative of elastin breakdown.The aim of this study was to apply a novel methodology, based on high-performance capillary electrophoresis, to the quantification of desmosine and isodesmosine in 11 patients with stable chronic obstructive pulmonary disease (COPD), 10 with an exacerbation of COPD, nine with a 1 -antitrypsin deficiency, 13 with bronchiectasis, and 11 adults with cystic fibrosis, in comparison to 24 controls.It was found that, in patients with stable COPD, urinary desmosine levels were higher than in controls (p=0.03), but lower than in COPD subjects with an exacerbation (p#0.05). The highest desmosine levels were found in subjects with a 1 -antitrypsin deficiency, bronchiectasis and cystic fibrosis (p<0.001 versus stable COPD). In a shortterm longitudinal study, five stable COPD patients showed a constant rate of desmosine excretion (mean coefficient of variation <8% over three consecutive days).In conclusion, the present method is simple and suitable for the determination of elastin-derived cross-linked amino acid excretion in urine, giving results similar to those obtained using other separation methods. In addition, evidence is presented that urinary desmosine excretion is increased in conditions characterized by airway inflammation, such as exacerbations of chronic obstructive pulmonary disease, bronchiectasis and cystic fibrosis. Results obtained in subjects with a 1 -antitrypsin deficiency suggest that this method might be used to evaluate the putative efficacy of replacement therapy. Eur Respir J 2000; 15: 1039±1045. Chronic obstructive pulmonary disease (COPD), with or without inherited deficiency of a 1 -antitrypsin (AAT), disseminated bronchiectasis (Bx) and cystic fibrosis (CF) are destructive lung disorders characterized by chronic and irreversible airflow limitation. Irrespective of the aetiological factors implicated, there is a solid body of evidence suggesting that degradation of the extracellular matrix component, mainly elastin, due to an imbalance between proteinases and their naturally occurring inhibitors, is central to many of the pathological features of these conditions [1±4].Excess lung elastin degradation results in the excretion of elastin-derived peptides containing desmosine (DES) and isodesmosine (IDES) in urine [5]. Since these crosslinked amino acids are unique to mature elastin, their urine levels are considered to be representative of body elastin breakdown. Urinary excretion of DES and IDES has been reported to be increased in patients with COPD, current smokers with normal lung function [6] and adults with CF [7] compared to appropriate controls.There are two validated means of detecting DES and IDES in body fluids: a separation method, based on isotope -dilution/high -performance liquid chromatography (HPLC) [8], and ...

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Section: Discussionmentioning

confidence: 99%

MEKC of desmosine and isodesmosine in urine of chronic destructive lung disease patients

Viglio¹,

Iadarola²,

Lupi³

et al. 2000

Eur Respir J

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“…Collagen content was determined with the chloramine T/paradimethylaminobenzaldehyde reaction as [(hydroxyproline content ϫ 7.46/protein content) ϫ 100] (25). Elastin and the elastin-specific, cross-linking amino acids desmosine and isodesmosine were assayed by capillary zone electrophoresis and UV detection (16).…”

Section: Methodsmentioning

confidence: 99%

The onset of left ventricular diastolic dysfunction in SHR rats is not related to hypertrophy or hypertension

Dupont

Maizel

Mentaverri

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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Dupont S, Maizel J, Mentaverri R, Chillon JM, Six I, Giummelly P, Brazier M, Choukroun G, Tribouilloy C, Massy ZA, Slama M. The onset of left ventricular diastolic dysfunction in SHR rats is not related to hypertrophy or hypertension. Am J Physiol Heart Circ Physiol 302: H1524 -H1532, 2012. First published January 27, 2012; doi:10.1152/ajpheart.00955.2010.-Left ventricular (LV) diastolic dysfunction, particularly relaxation abnormalities, are known to be associated with the development of LV hypertrophy (LVH). Preliminary human and animal studies suggested that early LV diastolic dysfunction may be revealed independently of LVH. However, whether LV diastolic dysfunction is compromised before the onset of hypertension and LVH remains unknown. We therefore evaluated LV diastolic function in spontaneously hypertensive rats (SHR) at different ages and tested whether LV diastolic dysfunction is associated with abnormal intracellular calcium homeostasis. LV systolic and diastolic functions were evaluated by invasive and echocardiographic methods in 3-week-old (without hypertension) and 5-week-old (with hypertension) SHR and Wistar-Kyoto control rats. Basal intracytoplasmic calcium and sarcoplasmic reticulum (SR) Ca 2ϩ contents were measured in cardiomyocytes using fura-2 AM. Sarco(endo)plasmic Ca 2ϩ -ATPase isoform 2a (SERCA 2a) and phospholamban (PLB) expressions were quantified by Western blot and quantitative RT-PCR techniques. LV relaxation dysfunction was observed in 3-week-old SHR rats before onset of hypertension and LVH. An increase in basal intracytoplasmic Ca 2ϩ and a decrease in SR Ca 2ϩ release were demonstrated in SHR. Decreased expression of SERCA 2a and Ser16 PLB (p16-PLB) protein levels was also observed in SHR rats, whereas mRNA expression was not decreased. For the first time, we have shown that LV myocardial dysfunction precedes hypertension in 3-week-old SHR rats. This LV myocardial dysfunction was associated with high diastolic [Ca 2ϩ ]i possibly due to decreased SERCA 2a and p16-PLB protein levels. Diastolic dysfunction may be a potential predictive marker of arterial hypertension in genetic hypertension syndromes.diastole; ultrasonic; calcium; spontaneously hypertensive rats LEFT VENTRICULAR (LV) DIASTOLIC dysfunction is responsible for more than one half of all hospitalizations for congestive heart failure or acute pulmonary oedema, which has been shown to be the consequence of multiple clinical factors, mostly hypertension (15). LV diastolic dysfunction, particularly relaxation abnormalities, is usually recognized to be closely associated with the development of left ventricular hypertrophy (LVH) in hypertensive humans and spontaneously hypertensive rats (SHR), a model of human genetic hypertension (35). Nevertheless, in a previous study, we demonstrated LV relaxation impairment in young SHR without LVH (37), subsequently confirmed by Aeschbacher et al (1). Di Bello et al. (13) have also demonstrated early LV diastolic dysfunction before the onset of hypertension and LVH. In view of these da...

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“…Aortic wall collagen, elastin, and the content of the elastin-specific cross-linking amino acids desmosine and isodesmosine were determined by capillary zone electrophoresis and ultraviolet detection after hydrochloric acid hydrolysis. 18 For technical reasons, this procedure could not be performed after 10 weeks of uremia.…”

Section: Histological Proceduresmentioning

confidence: 99%

Mechanisms of Aortic and Cardiac Dysfunction in Uremic Mice With Aortic Calcification

et al. 2009

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Background-Chronic renal failure (CRF) is associated with cardiac dysfunction and increased aortic stiffness. The mechanisms involved are not clearly understood. We examined changes over time in cardiac and aortic function in a murine CRF model. Methods and Results-Eight-week-old mice were randomly assigned to 1 of 4 groups: wild-type non-CRF, wild-type CRF, apolipoprotein E knockout non-CRF, and apolipoprotein E knockout CRF. Echocardiography was performed and blood samples were taken at baseline and after 6 and 10 weeks of CRF. Vascular reactivity and adhesion molecule expression were studied after 6 and 10 weeks of CRF. Left ventricular hypertrophy, altered left ventricular relaxation, and increased aortic stiffness were observed after 6 weeks of CRF and persisted after 10 weeks. The 4 groups of mice did not significantly differ in terms of arterial blood pressure and aortic structure. The degree of vascular calcification and serum total cholesterol concentration were higher in the CRF groups than in the non-CRF groups. These changes, however, could not explain the cardiac and vascular differences seen in the 2 CRF groups. In contrast, alterations in vascular reactivity, the upregulation of adhesion molecule expression, and CRF status were significantly associated with these changes. Conclusions-In a mouse model of CRF, left ventricular hypertrophy, cardiac diastolic dysfunction, and increased aortic stiffness were not related to structural changes in the aorta (including aortic calcification) or high serum cholesterol levels. However, cardiac and aortic abnormalities were associated with the extent of subendothelial dysfunction and the severity of CRF.

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Measurement of desmosine and isodesmosine by capillary zone electrophoresis

Cited by 22 publications

References 12 publications

MEKC of desmosine and isodesmosine in urine of chronic destructive lung disease patients

MEKC of desmosine and isodesmosine in urine of chronic destructive lung disease patients

The onset of left ventricular diastolic dysfunction in SHR rats is not related to hypertrophy or hypertension

Mechanisms of Aortic and Cardiac Dysfunction in Uremic Mice With Aortic Calcification

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