Premium
Suppression of fibrous adhesion by proteoglycan decorin
Author(s) -
Fukui Naoshi,
Fukuda Akira,
Kojima Kazunori,
Nakajima Kohei,
Oda Hiromi,
Nakamura Kozo
Publication year - 2001
Publication title -
journal of orthopaedic research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.041
H-Index - 155
eISSN - 1554-527X
pISSN - 0736-0266
DOI - 10.1016/s0736-0266(00)90016-0
Subject(s) - decorin , proteoglycan , adhesion , chemistry , cell adhesion , microbiology and biotechnology , transforming growth factor , extracellular matrix , biochemistry , biology , organic chemistry
Small proteoglycan decorin is known to suppress the bioactivity of TGF‐β through a competitive binding with the cell surface receptors for the cytokine. Based on this knowledge, we hypothesized that decorin could reduce the formation of fibrous adhesion, because our previous study showed the neutralizing antibody to TGF‐β1 has that effect. An intra‐articular adhesion model in the rabbit knee joint was employed in this study, and decorin was administered into the joint cavity continuously during the 4 weeks of the experiment. The results of the dose—response study demonstrated that decorin suppresses formation of fibrous adhesion in a dose‐dependent manner. When the administration of decorin was limited to shorter periods, this effect was considerably impaired and the necessity of long‐term administration was demonstrated. On the other hand, when administered together with TGF‐β1, decorin still suppressed adhesion but to a lesser extent, and it was suggested that this proteoglycan could have other significant mechanism(s) to suppress adhesion besides the neutralization of TGF‐β. Thus, the present study showed that decorin could inhibit adhesion formation by both TGF‐β dependent and independent mechanisms. Considering that decorin exists ubiquitously in the body, its administration might be a promising approach to suppress adhesion. © 2001 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved.