Vol.23 No.3

Original Article

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

Authors

Minako Murata1 , Kazuo Yudoh1 , Hiroyuki Shimizu2 , Moroe Beppu2 , Hiroshi Nakamura4 , Tomohiro Kato3 , Kayo Masuko3, 5

  • Department of Frontier Medicine, Institute of Medical Science, St. Marianna University School of Medicine, 2-16-1 Sugao, Miyamae-ku, Kawasaki-shi Kanagawa, 216-8511, Japan
  • Department of Orthopedic Surgery, St. Marianna University School of Medicine, 2-16-1 Sugao, Miyamae-ku, Kawasaki-shi Kanagawa, 216-8511, Japan
  • Department of Biochemistry, St. Marianna University School of Medicine, 2-16-1 Sugao, Miyamae-ku, Kawasaki-shi Kanagawa, 216-8511, Japan
  • Department of Joint Disease and Rheumatism, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8603, Japan
  • Graduate School of Nutritional Science, Sagami Women’s University, Bunkyo 2-1-1, Minami-ku, Sagamihara-shi Kanagawa, 252-0383, Japan
Received:

14 March 2012

Accepted:

28 May 2012

Published online:

22 June 2012

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Abstract

Objective 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.
Methods Samples were obtained from patients undergoing joint arthroplasty. Cells were grown in vitro, then stimulated with interleukin (IL)-1b or tumor necrosis factor alpha (TNFa) 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-1b, and then analyzed the production of matrix metalloproteinase (MMP)-1 and MMP-13 in the
treated chrondrocytes. Results The results showed that LAYN was constitutively expressed in human articular chondrocytes and synoviocytes and that IL-1b significantly suppressed the expression of LAYN in these cells. HA repressed IL-1b-induced MMP-1 and MMP-13 production in chondrocytes, but this was significantly abrogated in chondrocytes transfected with siRNA against LAYN.
Conclusions 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.

Key words

Layilin, Hyaluronan, Arthritic chondrocyte, Interleukin-1, Matrix metalloproteinase