Thioredoxin Gene Expression in Rat Knee Articular Cartilage After Full-Thickness Injury

• Published in: Connective Tissue Research Vol. 46; no. 1; pp. 27 - 32
• Main Authors: Kakimaru, Hiroyuki, Kataoka, Hiroko, Enomoto, Koh-ichi, Kumahashi, Nobuyuki, Ohira, Akihiro, Yodoi, Junji, Uchio, Yuji, Ochi, Mitsuo
• Format: Journal Article
• Language: English
• Published: England Informa UK Ltd 01.01.2005; Taylor & Francis
• Subjects: Animals; Articular Cartilage; Cartilage Injury; Cartilage, Articular - injuries; Cartilage, Articular - metabolism; Cartilage, Articular - pathology; Expression; Extremities - injuries; Extremities - pathology; FullThickness Defect; Gene Expression Regulation - genetics; In Situ Hybridization; Joints - injuries; Joints - metabolism; Joints - pathology; Male; Rats; Rats, Wistar; RNA, Messenger - genetics; Thioredoxin; Thioredoxins - genetics; Thioredoxins - metabolism; trx
• ISSN: 0300-8207; 1521-0456; 1607-8438
• DOI: 10.1080/03008200590935529

To study the expression of the antioxidative protein thioredoxin (TRX) in intact and injured articular cartilage, we examined the presence of trxmRNA in rat knee joints by in situ hybridization. Our results showed that in the intact knee, most cells, including articular cartilage chondrocytes, expressed trx mRNA. We examined joints at 1, 7, 14, and 28 days after the infliction of full-thickness cartilage injuries on distal femoral condyles. At 1 day after injury, no significant changes were observed in the wound or in trx expression pattern. However, at 7 to 28 days after injury, the wound became filled with repair tissue. Also, trx expression was detected in differentiating mesenchymal cells in the deeper zones of the wound but not in fibroblast-like cells in the upper part of the repair tissue, toward the joint cavity. This lack of TRX expression in the fibroblast-like cells may underlie the susceptibility of the repair tissue fibrocartilage to oxidative stress.