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Mediation of Cartilage Matrix Degeneration and Fibrillation by Decorin in Post-traumatic Osteoarthritis
Journal article   Open access

Mediation of Cartilage Matrix Degeneration and Fibrillation by Decorin in Post-traumatic Osteoarthritis

Qing Li, Biao Han, Chao Wang, Wei Tong, Yulong Wei, Wei-Ju Tseng, Li-Hsin Han, X Sherry Liu, Motomi Enomoto-Iwamoto, Robert L Mauck, …
Arthritis & rheumatology (Hoboken, N.J.), v 72(8), pp 1266-1277
Aug 2020
PMID: 32162789
url
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7486252View
Accepted (AM)Open Access (License Unspecified) Open

Abstract

Aggrecans - metabolism Animals Cartilage, Articular - metabolism Chondrocytes - metabolism Collagen - metabolism Decorin - metabolism Disease Models, Animal Glycosaminoglycans - metabolism Interleukin-1beta - metabolism Matrilin Proteins - metabolism Menisci, Tibial - metabolism Mice Mice, Knockout Osteoarthritis - etiology Osteoarthritis - metabolism Osteophyte - metabolism Wounds and Injuries - complications
To elucidate the role of decorin, a small leucine-rich proteoglycan, in the degradation of cartilage matrix during the progression of post-traumatic osteoarthritis (OA). Three-month-old decorin-null (Dcn ) and inducible decorin-knockout (Dcn ) mice were subjected to surgical destabilization of the medial meniscus (DMM) to induce post-traumatic OA. The OA phenotype that resulted was evaluated by assessing joint morphology and sulfated glycosaminoglycan (sGAG) staining via histological analysis (n = 6 mice per group), surface collagen fibril nanostructure via scanning electron microscopy (n = 4 mice per group), tissue modulus via atomic force microscopy-nanoindentation (n = 5 or more mice per group) and subchondral bone structure via micro-computed tomography (n = 5 mice per group). Femoral head cartilage explants from wild-type and Dcn mice were stimulated with the inflammatory cytokine interleukin-1β (IL-1β) in vitro (n = 6 mice per group). The resulting chondrocyte response to IL-1β and release of sGAGs were quantified. In both Dcn and Dcn mice, the absence of decorin resulted in accelerated sGAG loss and formation of highly aligned collagen fibrils on the cartilage surface relative to the control (P < 0.05). Also, Dcn mice developed more salient osteophytes, illustrating more severe OA. In cartilage explants treated with IL-1β, loss of decorin did not alter the expression of either anabolic or catabolic genes. However, a greater proportion of sGAGs was released to the media from Dcn mouse explants, in both live and devitalized conditions (P < 0.05). In post-traumatic OA, decorin delays the loss of fragmented aggrecan and fibrillation of cartilage surface, and thus, plays a protective role in ameliorating cartilage degeneration.

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Collaboration types
Domestic collaboration
Web of Science research areas
Rheumatology
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