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A friend in knee: CCN3 may inhibit osteoarthritis progression

Osteoarthritis (OA) is a major clinical problem among the ageing population, yet no disease-modifying treatments currently exist. This issue arises, in part, due to the complex processes occurring in the microenvironment of articular cartilage that lead to osteoarthritic changes. Gaining a better un...

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Detalles Bibliográficos
Autor principal: Peidl, Alex
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Netherlands 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5910325/
https://www.ncbi.nlm.nih.gov/pubmed/29332174
http://dx.doi.org/10.1007/s12079-017-0446-y
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author Peidl, Alex
author_facet Peidl, Alex
author_sort Peidl, Alex
collection PubMed
description Osteoarthritis (OA) is a major clinical problem among the ageing population, yet no disease-modifying treatments currently exist. This issue arises, in part, due to the complex processes occurring in the microenvironment of articular cartilage that lead to osteoarthritic changes. Gaining a better understanding of these processes is crucial in developing a viable therapy for OA. A recent report in Journal of Bone Mineral Metabolism by Janune et al. (J Bone Miner Metab 35:582–597, 2016) suggests a novel role for CCN3 in maintaining the differentiated phenotype of articular cartilage. This report suggests that CCN3, a member of the CCN family of matricellular proteins, is important for proteoglycan accumulation, as well as expression of type II collagen, tenascin C, and lubricin in vitro. Furthermore, exogenous CCN3 increased tidemark integrity and lubricin protein expression in a rat model of OA. These results implicate the regulation of CCN3 as a potential therapeutic target in patients with OA.
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spelling pubmed-59103252018-04-24 A friend in knee: CCN3 may inhibit osteoarthritis progression Peidl, Alex J Cell Commun Signal Bits and Bytes Osteoarthritis (OA) is a major clinical problem among the ageing population, yet no disease-modifying treatments currently exist. This issue arises, in part, due to the complex processes occurring in the microenvironment of articular cartilage that lead to osteoarthritic changes. Gaining a better understanding of these processes is crucial in developing a viable therapy for OA. A recent report in Journal of Bone Mineral Metabolism by Janune et al. (J Bone Miner Metab 35:582–597, 2016) suggests a novel role for CCN3 in maintaining the differentiated phenotype of articular cartilage. This report suggests that CCN3, a member of the CCN family of matricellular proteins, is important for proteoglycan accumulation, as well as expression of type II collagen, tenascin C, and lubricin in vitro. Furthermore, exogenous CCN3 increased tidemark integrity and lubricin protein expression in a rat model of OA. These results implicate the regulation of CCN3 as a potential therapeutic target in patients with OA. Springer Netherlands 2018-01-13 2018-06 /pmc/articles/PMC5910325/ /pubmed/29332174 http://dx.doi.org/10.1007/s12079-017-0446-y Text en © The Author(s) 2018 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Bits and Bytes
Peidl, Alex
A friend in knee: CCN3 may inhibit osteoarthritis progression
title A friend in knee: CCN3 may inhibit osteoarthritis progression
title_full A friend in knee: CCN3 may inhibit osteoarthritis progression
title_fullStr A friend in knee: CCN3 may inhibit osteoarthritis progression
title_full_unstemmed A friend in knee: CCN3 may inhibit osteoarthritis progression
title_short A friend in knee: CCN3 may inhibit osteoarthritis progression
title_sort friend in knee: ccn3 may inhibit osteoarthritis progression
topic Bits and Bytes
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5910325/
https://www.ncbi.nlm.nih.gov/pubmed/29332174
http://dx.doi.org/10.1007/s12079-017-0446-y
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