Layilin, a talin-binding hyaluronan receptor, is expressed in human articular chondrocytes and synoviocytes and is down-regulated by interleukin-1β

被引:12
|
作者
Murata, Minako [1 ]
Yudoh, Kazuo [1 ]
Shimizu, Hiroyuki [2 ]
Beppu, Moroe [2 ]
Nakamura, Hiroshi [3 ]
Kato, Tomohiro [4 ]
Masuko, Kayo [4 ,5 ]
机构
[1] St Marianna Univ, Sch Med, Dept Frontier Med, Inst Med Sci,Miyamae Ku, Kawasaki, Kanagawa 2168511, Japan
[2] St Marianna Univ, Sch Med, Dept Orthoped Surg, Miyamae Ku, Kawasaki, Kanagawa 2168511, Japan
[3] Nippon Med Sch, Dept Joint Dis & Rheumatism, Bunkyo Ku, Tokyo 1138603, Japan
[4] St Marianna Univ, Sch Med, Dept Biochem, Miyamae Ku, Kawasaki, Kanagawa 2168511, Japan
[5] Sagami Womens Univ, Grad Sch Nutr Sci, Minami Ku, Sagamihara, Kanagawa 2520383, Japan
关键词
Layilin; Hyaluronan; Arthritic chondrocyte; Interleukin-1; Matrix metalloproteinase; GENE-EXPRESSION; CD44; INJECTIONS; OSTEOARTHRITIS; CYTOKINES; PROTEIN; MMP-1; ACID; KNEE;
D O I
10.1007/s10165-012-0686-x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Layilin (LAYN), a 55-kDa transmembrane protein with homology to C-type lectins, has been identified as a receptor of hyaluronan (HA). Interestingly, LAYN does not share any sequence homology with CD44, a primary HA receptor. The primary aim of our study was to examine the expression and potential function of LAYN in human articular chondrocytes and synoviocytes. Samples were obtained from patients undergoing joint arthroplasty. Cells were grown in vitro, then stimulated with interleukin (IL)-1 beta or tumor necrosis factor alpha (TNF alpha) for 24 h and the expression of LAYN was analyzed. To assess the function of LAYN, we transfected chondrocytes with siRNA against LAYN, treated them with HA and IL-1 beta, and then analyzed the production of matrix metalloproteinase (MMP)-1 and MMP-13 in the treated chrondrocytes. The results showed that LAYN was constitutively expressed in human articular chondrocytes and synoviocytes and that IL-1 beta significantly suppressed the expression of LAYN in these cells. HA repressed IL-1 beta-induced MMP-1 and MMP-13 production in chondrocytes, but this was significantly abrogated in chondrocytes transfected with siRNA against LAYN. Our results show that human chondrocytes express LAYN, a novel HA receptor, and that LAYN may contribute to the regulation of HA functions in the arthritic condition. Further investigation of the HA receptor may lead to the development of novel therapeutics to regulate HA signaling in inflammatory arthritis.
引用
收藏
页码:478 / 488
页数:11
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