Plasma and urinary glycosaminoglycans in the course of juvenile idiopathic arthritis

Winsz-Szczotka, Katarzyna; Kuźnik-Trocha, Kornelia; Komosińska-Vassev, Katarzyna; Wisowski, Grzegorz; Gruenpeter, Anna; Lachór-Motyka, Iwona; Żegleń, Bogusław; Lemski, Wojciech; Olczyk, Krystyna

doi:10.1016/j.bbrc.2015.02.018

Cited by 11 publications

(33 citation statements)

References 36 publications

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“…Taken together, these results show that the modulation of HS in the ECM and on cell membranes is crucial for the initiation of inflammation and fibrosis. However, if we look into inflammation and matrix remodelling processes, young patients with juvenile idiopathic arthritis have similar HS plasma and urinary concentrations compared to healthy controls [51]. It is probable that it is not only the presence of HS that determines function but also its sulfation pattern.…”

Section: Enzymes Involved In Hs Modificationmentioning

confidence: 99%

Mechanisms of Renal Graft Chronic Injury and Progression to Interstitial Fibrosis

et al. 2015

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Following transplantation, the kidney is exposed to many different injuries which result in inflammation, overproduction of extracellular matrix, interstitial fibrosis and progressive loss of renal function. To date, treatment options for patients with progressive graft dysfunction are very limited. The development of new therapies requires a better understanding of the pathogenesis of transplant interstitial fibrosis and specific biomarkers to identify patients with progressive transplant fibrosis and monitor response to new therapies. Here, we review our current understanding of how and why extracellular matrix accumulates and the relationship between fibrosis and inflammation. In particular, we focus on the role of heparan sulphate that regulates recruitment, migration and differentiation of interstitial cells and also acts as a reservoir for multiple cytokines and growth factors.

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Section: Enzymes Involved In Hs Modificationmentioning

confidence: 99%

Mechanisms of Renal Graft Chronic Injury and Progression to Interstitial Fibrosis

et al. 2015

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“…Metabolic alterations of extracellular matrix (ECM) components have been shown to play a considerable role in pathological changes in the course of JIA [4,13,15,16].…”

Section: Introductionmentioning

confidence: 99%

“…PGs have been classified according to their core proteins, localization and GAGs composition. The GAGs chains on the protein core are unbranched polysaccharide chains composed of repeating disaccharide units that can be further divided into sulfated and non-sulfated GAGs [2,16]. Sulfated GAGs include chondroitin sulfate A (or chondroitin-4-sulfate), chondroitin sulfate C (or chondroitin-6-sulfate) and highly sulphonated GAGs (or heparan sulfate and keratan sulfate (KS)).…”

Section: Introductionmentioning

confidence: 99%

Connective Tissue Metabolism in Patients With Juvenile Idiopathic Arthritis: 10-Year Follow-Up Study

Panko

Shevchenko

Rakovska

et al. 2019

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CONNECTIVE TISSUE METABOLISM IN PATIENTS WITH JUVENILE IDIOPATHIC ARTHRITIS: 10-YEAR FOLLOW-UP STUDYShevchenko N.S., Panko N.O., Rakovska L.O., Holovko T.O. Connective tissue remodeling is essential for progressive course of juvenile idiopathic arthritis (JIA), therefore changes in glucosaminoglycans (GAGs) fractions with time in patients with JIA have been studied during 10-year follow-up. The study involved 22 healthy children (controls) and 83 patients with JIA aged from 2 to 18. The follow‑up study was yearly held for 10 years and initially included 14 patients with JIA investigated for connective tissue metabolism. Proteoglycans metabolism in children with JIA is characterized by a decrease in the total GAGs, mainly by means of low levels of chondroitin-4-sulfate and highly sulphonated GAGs. This redistribution was more specific for children with prolonged disease duration (more than 5 years). Slowing of proteoglycans metabolism in reducing the excretion of uronic acids was the most common for up to 2 years of disease duration as compared to later stages. The severity of metabolic imbalance of proteoglycans depends on the duration of JIA and has the most unfavorable period of 5 years and later after the onset of the disease.Keywords: juvenile idiopathic arthritis, connective tissue metabolism. МЕТАБОЛІЗМ СПОЛУЧНОЇ ТКАНИНИ У ПАЦІЄНТІВ ІЗ ЮВЕНІЛЬНИМ ІДІОПАТИЧНИМ АРТРИТОМ: 10-РІЧНИЙ КАТАМНЕЗ.Шевченко Н.С., Панько Н.О., Раковська Л.О., Головко Т.О. Ремоделювання сполучної тканини є важливою складовою прогресуючого перебігу ювенільного ідіопатичного артриту (ЮІА), тому метою даного дослідження було вивчення динаміки змін з боку окремих фракцій глюкозаміногліканів (ГАГ) у пацієнтів з ЮІА впродовж 10 років. Дослідження включало 83 пацієнта з ЮІА віком від 2 до 18 років і 22 здорові дитини порівнюваних за віком та статтю. Катамнестичне спостереження проводилося протягом 10 років і спочатку стартувало з обстеження сполучнотканинного обміну у 14 хворих на ЮІА, показники якого у подальшому контролювалися в динаміці. В результаті дослідження було виявлено, що метаболізм протеогліканів у дітей з ЮІА характеризувався зниженням загального рівня ГАГ, в основному за рахунок хондроїтин-4-сульфату і високосульфанізованих ГАГ. Дана тенденція була найбільш характерною для доволі пізніх строків розвитку ЮІА (при анамнезі більше 5 років). Уповільнення обміну протеогліканів, про що свідчило зниження екскреції уронових кислот, найбільш часто виявлялося в період до 2 років у порівнянні з більш пізніми термінами перебігу хвороби.Таким чином, зміни сполучнотканинного обміну залежали від тривалості захворювання і були найбільш виражені в період 5 років і більше від початку захворювання.Ключові слова: ювенільний ідіопатичний артрит, обмін сполучної тканини. МЕТАБОЛИЗМ СОЕДИНИТЕЛЬНОЙ ТКАНИ У ПАЦИЕНТОВ С ЮВЕНИЛЬНЫМ ИДИОПАТИЧЕСКИМ АРТРИТОМ: 10-ЛЕТНИЙ КАТАМНЕЗ.Шевченко Н.С., Панько Н.А., Раковская Л.А., Головко Т.А. Ремоделирование соединительной ткани является важной составляющей прогрессирующего течения ювенильного идиопатического артрита (ЮИА), поэтому целью данного исследования было изучение динамики изменений со стороны отдельных фракций глюкозаминогликанов (ГАГ) у пациентов с ЮИА на протяжении 10 лет.Исследование включало 83 пациента с ЮИА возрастом от 2 до 18 лет и 22 здоровых ребенка сопоставимых по возрасту и полу. Катамнестическое наблюдение проводилось в течение 10 лет и изначально стартовало с обследования соединительно-тканного обмена у 14 детей с ЮИА, который в последующем контролировался в динамике. В результате исследования было выявлено, что метаболизм протеогликанов у детей с ЮИА характеризуется снижением общего уровня ГАГ, в основном за счет хондроитин-4-сульфата и высокосульфанизированных ГАГ. Данная тенденция была наиболее характерной для более позних сроков ЮИА (при анамнезе более 5 лет). Замедление обмена протеогликанов, о чем свидетельствовало снижение экскреции уроновых кислот, наиболее часто выявлялось в период до 2 лет в сравнении с более поздними сроками развития болезни.Таким образом, изменения соединительно-тканного обмена зависели от длительности заболевания и были наиболее выражены в период 5 лет и более от начала заболевания. Ключевые слова: ювенильный идиопатический артрит, обмен соединительной ткани.

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“…The results of this work indicate that leptin and adiponectin but not resistin may be involved in the development and progression of joint dysfunction in JIA. Additionally, we suggest that YKL-40 may be a useful biomarker of disease activity and may be used to assess treatment towards remission, as compared to COMP.Metabolites 2020, 10, 61 2 of 11 remodeling, manifested by significant changes of the circulating markers of cartilage turnover, including total glycosaminoglycans (GAGs) and their particular types such as keratan sulphate, chondroitin sulphate, hyaluronic acid, as well as chondroitin sulphate 846 epitope [5][6][7][8].Among ECM components, which are indicators of the cartilage breakdown, there are also listed components synthesized by chondrocytes, i.e., cartilage oligomeric matrix protein (COMP) as well as human cartilage glycoprotein 39 (YKL-40), that are so far not evaluated in JIA patients. The first one is a non-collagenous glycoprotein, binding to aggrecan; fibronectin; and collagen types I, II, and IX, which seem to play a role in the structure of fibrils and in maintenance of the collagen network [9,10].…”

mentioning

confidence: 99%

“…Metabolites 2020, 10, 61 2 of 11 remodeling, manifested by significant changes of the circulating markers of cartilage turnover, including total glycosaminoglycans (GAGs) and their particular types such as keratan sulphate, chondroitin sulphate, hyaluronic acid, as well as chondroitin sulphate 846 epitope [5][6][7][8].…”

mentioning

confidence: 99%

Association of Circulating COMP and YKL-40 as Markers of Metabolic Changes of Cartilage with Adipocytokines in Juvenile Idiopathic Arthritis

Winsz-Szczotka

Kuźnik-Trocha

Gruenpeter³

et al. 2020

Metabolites

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The aim of this study was to evaluate the association of circulating cartilage oligomeric matrix protein (COMP) and human cartilage glycoprotein-39 (YKL-40) as markers of metabolic changes of cartilage, with leptin, adiponectin, and resistin in juvenile idiopathic arthritis (JIA) patients before and after treatment. A significant decrease of COMP and an increase of YKL-4 were found in blood of untreated patients. JIA treatment leading to clinical improvement resulted in normalization of COMP levels only. Concentrations of both markers in treated patients, while showing no clinical improvement, differed from those in controls and patients with remission. The leptin level decreased (p < 0.05) in untreated patients; however, concentrations of adiponectin and resistin increased (p < 0.05) as compared to controls. JIA treatment resulted in normalization of adipocytokine levels in remissive patients but not those with active JIA. Untreated patients showed a correlation between COMP and leptin, adiponectin, and body mass index (BMI) and between YKL-40 and leptin, adiponectin, BMI, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR). In inactive JIA, a correlation between YKL-40 and leptin was shown. Treated patients with an active JIA demonstrated a correlation between COMP and adiponectin and between YKL-40 and leptin, adiponectin, BMI, CRP, and ESR. The results of this work indicate that leptin and adiponectin but not resistin may be involved in the development and progression of joint dysfunction in JIA. Additionally, we suggest that YKL-40 may be a useful biomarker of disease activity and may be used to assess treatment towards remission, as compared to COMP.Metabolites 2020, 10, 61 2 of 11 remodeling, manifested by significant changes of the circulating markers of cartilage turnover, including total glycosaminoglycans (GAGs) and their particular types such as keratan sulphate, chondroitin sulphate, hyaluronic acid, as well as chondroitin sulphate 846 epitope [5][6][7][8].Among ECM components, which are indicators of the cartilage breakdown, there are also listed components synthesized by chondrocytes, i.e., cartilage oligomeric matrix protein (COMP) as well as human cartilage glycoprotein 39 (YKL-40), that are so far not evaluated in JIA patients. The first one is a non-collagenous glycoprotein, binding to aggrecan; fibronectin; and collagen types I, II, and IX, which seem to play a role in the structure of fibrils and in maintenance of the collagen network [9,10]. Whereas YKL-40, a glycoprotein associated with inflammation and tissue remodeling, is produced by joint tissues and recognized as a candidate autoantigen in rheumatoid arthritis. It has been shown that YKL-40 binds to some important components in the cartilage extracellular matrix, i.e., proteoglycans and collagens, influencing their production and assembly [11][12][13][14]. Several authors have investigated the relationship between circulating COMP or YKL-40 and the condition of articular cartilage in adult patients with and without any r...

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Plasma and urinary glycosaminoglycans in the course of juvenile idiopathic arthritis

Cited by 11 publications

References 36 publications

Mechanisms of Renal Graft Chronic Injury and Progression to Interstitial Fibrosis

Mechanisms of Renal Graft Chronic Injury and Progression to Interstitial Fibrosis

Connective Tissue Metabolism in Patients With Juvenile Idiopathic Arthritis: 10-Year Follow-Up Study

Association of Circulating COMP and YKL-40 as Markers of Metabolic Changes of Cartilage with Adipocytokines in Juvenile Idiopathic Arthritis

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