YKL-40 as a Novel Factor Associated with Inflammation and Catabolic Mechanisms in Osteoarthritic Joints

YKL-40 is associated with tissue injury and inflammation, and consequently to diseases in which these mechanisms lead to tissue degradation, for example, asthma and rheumatoid arthritis. The purpose of the present study was to investigate if YKL-40 is also a significant factor in osteoarthritis (OA)...

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Main Authors: Tuija Väänänen, Anna Koskinen, Erja-Leena Paukkeri, Mari Hämäläinen, Teemu Moilanen, Eeva Moilanen, Katriina Vuolteenaho
Format: Article
Language:English
Published: Hindawi Limited 2014-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2014/215140
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spelling doaj-c4b53422d9844dd9a0db7298d0e718f12020-11-25T00:15:20ZengHindawi LimitedMediators of Inflammation0962-93511466-18612014-01-01201410.1155/2014/215140215140YKL-40 as a Novel Factor Associated with Inflammation and Catabolic Mechanisms in Osteoarthritic JointsTuija Väänänen0Anna Koskinen1Erja-Leena Paukkeri2Mari Hämäläinen3Teemu Moilanen4Eeva Moilanen5Katriina Vuolteenaho6The Immunopharmacology Research Group, University of Tampere School of Medicine and Tampere University Hospital, 33014 Tampere, FinlandThe Immunopharmacology Research Group, University of Tampere School of Medicine and Tampere University Hospital, 33014 Tampere, FinlandThe Immunopharmacology Research Group, University of Tampere School of Medicine and Tampere University Hospital, 33014 Tampere, FinlandThe Immunopharmacology Research Group, University of Tampere School of Medicine and Tampere University Hospital, 33014 Tampere, FinlandThe Immunopharmacology Research Group, University of Tampere School of Medicine and Tampere University Hospital, 33014 Tampere, FinlandThe Immunopharmacology Research Group, University of Tampere School of Medicine and Tampere University Hospital, 33014 Tampere, FinlandThe Immunopharmacology Research Group, University of Tampere School of Medicine and Tampere University Hospital, 33014 Tampere, FinlandYKL-40 is associated with tissue injury and inflammation, and consequently to diseases in which these mechanisms lead to tissue degradation, for example, asthma and rheumatoid arthritis. The purpose of the present study was to investigate if YKL-40 is also a significant factor in osteoarthritis (OA) by assessing associations of YKL-40 with mediators related to the pathogenesis of OA: cartilage destructing matrix metalloproteinases (MMPs) and proinflammatory cytokines interleukin-6 (IL-6) and interleukin-17 (IL-17). Cartilage, synovial fluid (SF), and plasma samples were obtained from 100 OA patients undergoing total knee replacement surgery. SF levels of YKL-40 (1027.9 ± 78.3 ng/mL) were considerably higher than plasma levels (67.2 ± 4.5 ng/mL) and correlated with YKL-40 released from cartilage samples obtained from the same patients (r=0.37, P=0.010), indicating that YKL-40 is produced by OA cartilage. Interestingly, YKL-40 concentrations in OA SF correlated positively with MMP-1 (r=0.36, P=0.014), MMP-3 (r=0.46, P=0.001), IL-6 (r=0.57, P<0.001), and IL-17 (r=0.52, P=0.010) levels. Moreover, IL-6 and IL-17 enhanced YKL-40 production in human primary chondrocyte cultures. The present study introduces YKL-40 as a cartilage-derived factor associated with mediators of inflammation and cartilage destruction involved in the pathogenesis of OA.http://dx.doi.org/10.1155/2014/215140
collection DOAJ
language English
format Article
sources DOAJ
author Tuija Väänänen
Anna Koskinen
Erja-Leena Paukkeri
Mari Hämäläinen
Teemu Moilanen
Eeva Moilanen
Katriina Vuolteenaho
spellingShingle Tuija Väänänen
Anna Koskinen
Erja-Leena Paukkeri
Mari Hämäläinen
Teemu Moilanen
Eeva Moilanen
Katriina Vuolteenaho
YKL-40 as a Novel Factor Associated with Inflammation and Catabolic Mechanisms in Osteoarthritic Joints
Mediators of Inflammation
author_facet Tuija Väänänen
Anna Koskinen
Erja-Leena Paukkeri
Mari Hämäläinen
Teemu Moilanen
Eeva Moilanen
Katriina Vuolteenaho
author_sort Tuija Väänänen
title YKL-40 as a Novel Factor Associated with Inflammation and Catabolic Mechanisms in Osteoarthritic Joints
title_short YKL-40 as a Novel Factor Associated with Inflammation and Catabolic Mechanisms in Osteoarthritic Joints
title_full YKL-40 as a Novel Factor Associated with Inflammation and Catabolic Mechanisms in Osteoarthritic Joints
title_fullStr YKL-40 as a Novel Factor Associated with Inflammation and Catabolic Mechanisms in Osteoarthritic Joints
title_full_unstemmed YKL-40 as a Novel Factor Associated with Inflammation and Catabolic Mechanisms in Osteoarthritic Joints
title_sort ykl-40 as a novel factor associated with inflammation and catabolic mechanisms in osteoarthritic joints
publisher Hindawi Limited
series Mediators of Inflammation
issn 0962-9351
1466-1861
publishDate 2014-01-01
description YKL-40 is associated with tissue injury and inflammation, and consequently to diseases in which these mechanisms lead to tissue degradation, for example, asthma and rheumatoid arthritis. The purpose of the present study was to investigate if YKL-40 is also a significant factor in osteoarthritis (OA) by assessing associations of YKL-40 with mediators related to the pathogenesis of OA: cartilage destructing matrix metalloproteinases (MMPs) and proinflammatory cytokines interleukin-6 (IL-6) and interleukin-17 (IL-17). Cartilage, synovial fluid (SF), and plasma samples were obtained from 100 OA patients undergoing total knee replacement surgery. SF levels of YKL-40 (1027.9 ± 78.3 ng/mL) were considerably higher than plasma levels (67.2 ± 4.5 ng/mL) and correlated with YKL-40 released from cartilage samples obtained from the same patients (r=0.37, P=0.010), indicating that YKL-40 is produced by OA cartilage. Interestingly, YKL-40 concentrations in OA SF correlated positively with MMP-1 (r=0.36, P=0.014), MMP-3 (r=0.46, P=0.001), IL-6 (r=0.57, P<0.001), and IL-17 (r=0.52, P=0.010) levels. Moreover, IL-6 and IL-17 enhanced YKL-40 production in human primary chondrocyte cultures. The present study introduces YKL-40 as a cartilage-derived factor associated with mediators of inflammation and cartilage destruction involved in the pathogenesis of OA.
url http://dx.doi.org/10.1155/2014/215140
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