Open AccessA friend in knee: CCN3 may inhibit osteoarthritis progression
Author(s) -
Peidl Alex
Publication year - 2018
Publication title -
journal of cell communication and signaling
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 44
eISSN - 1873-961X
pISSN - 1873-9601
DOI - 10.1007/s12079-017-0446-y
Subject(s) - osteoarthritis , medicine , matricellular protein , cartilage , proteoglycan , bioinformatics , phenotype , population , tenascin c , articular cartilage , pathology , cancer research , extracellular matrix , microbiology and biotechnology , biology , anatomy , immunohistochemistry , gene , genetics , alternative medicine , environmental health
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.