基于生化标记和组织学评价的组织蛋白酶K在猴子胶原诱导关节炎模型中的作用

IF 2.3 Q2 RHEUMATOLOGY International Journal of Rheumatology Pub Date : 2016-02-02 DOI:10.1155/2016/8938916
Makoto Tanaka, H. Yamada, S. Nishikawa, H. Mori, Y. Ochi, N. Horai, Minqi Li, N. Amizuka
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引用次数: 9

摘要

采用生化标记和组织学方法研究了组织蛋白酶K在食蟹猴胶原诱导关节炎(CIA)模型中关节降解中的作用。分析关节肿胀、尿II型胶原c端肽(CTX-II)、脱氧吡啶啉(DPD)、I型胶原N端肽和c端肽(NTX和CTX-I)。在关节处进行II型胶原、组织蛋白酶K和CTX-II的免疫组化。关节肿胀在第42天达到高峰,并持续到这个水平。CTX-II水平在第28天达到峰值,随后下降,而CTX-I、NTX和DPD在第43天达到平稳期。关节肿胀与第20天和第42/43天CTX-II升高呈正相关,与第42/43天和第84天CTX-I和NTX/Cr升高呈正相关,与整个研究期间DPD升高呈正相关。破骨细胞、关节软骨和滑膜组织中观察到强烈的组织蛋白酶K染色。CTX-II存在于CIA猴关节软骨的浅层。生化标志物的证据表明,CIA模型中的基质降解始于软骨的降解,而不是骨吸收。组织蛋白酶K在破骨细胞、关节软骨和滑膜组织中的表达可能有助于软骨的降解。
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Joint Degradation in a Monkey Model of Collagen-Induced Arthritis: Role of Cathepsin K Based on Biochemical Markers and Histological Evaluation
The role of cathepsin K in joint degradation in a model of collagen-induced arthritis (CIA) in cynomolgus monkey was examined using biochemical markers and histology. Joint swelling, urinary C-telopeptide of type II collagen (CTX-II), deoxypyridinoline (DPD), and N- and C-telopeptides of type I collagen (NTX and CTX-I, resp.) were analyzed. Immunohistochemistry of type II collagen, cathepsin K, and CTX-II were performed using joints. Joint swelling reached peak on day 42 and continued at this level. The CTX-II level peaked on day 28 and declined thereafter, while CTX-I, NTX, and DPD reached plateau on day 43. Joint swelling was positively correlated with CTX-II increases on days 20 and 42/43, with increases in CTX-I and NTX/Cr on days 42/43 and 84, and with DPD increases throughout the study period. Intense cathepsin K staining was observed in osteoclasts and in articular cartilage and synovial tissue in arthritic joints. CTX-II was present in the superficial layer of articular cartilage in CIA monkeys. Evidence from biochemical markers suggests that matrix degradation in the CIA model starts with degradation of cartilage, rather than bone resorption. Cathepsin K expressed in osteoclasts, articular cartilage, and synovial tissue may contribute to degradation of cartilage.
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来源期刊
CiteScore
4.40
自引率
0.00%
发文量
9
审稿时长
24 weeks
期刊最新文献
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