Abstract
Purpose: The hallmark of osteoarthritis (OA) is the continuous degradation of the cartilage extracellular matrix (ECM). Cartilage oligomeric matrix protein (COMP or thrombospondin-5) is ubiquitously expressed in the ECM of healthy cartilage, degraded in early OA, and re-expressed at a late stage of disease. The role of COMP is besides its cross-linking and stabilizing effect on the ECM still elusive. We hypothesized that in OA another ECM protein might compensate for the loss of COMP. Thrombospondin-4 (TSP-4), another member of the thrombospondin family and structurally similar to COMP, is known to be upregulated in injured tissues and associated with matrix remodeling and angiogenesis, could be such a candidate.
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