Total for the last 12 months
number of access : ?
number of downloads : ?
ID 25703
Author
Ikeda, Yuichi Department of Orthopedic Surgery, The University of Tokushima School of Medicine
Ikata, Takaaki Department of Orthopedic Surgery, The University of Tokushima School of Medicine
Mishiro, Takuya Department of Orthopedic Surgery, The University of Tokushima School of Medicine
Nakano, Shunji Department of Orthopedic Surgery, The University of Tokushima School of Medicine
Ikebe, Mitsugu Department of Orthopedic Surgery, The University of Tokushima School of Medicine
Yasuoka, Susumu Department of Nursing, The University of Tokushima School of Medical Sciences
Keywords
synovial fluid
cysteine protease
cathepsin B
rheumatoid arthritis
pro-urokinase
Content Type
Journal Article
Description
To clarify the pathophysiological role of cathepsins in rheumatoid arthritis (RA), we investigated whether cathepsin B or cathepsin L was increased in synovial fluid (SF) of RA joints, and whether the cathepsin isolated from SF of RA patients activated pro-urokinase or not. Thus, we estimated the content of cathepsins in SF of RA patients by measuring their activities by fluorospectrometry, using Z-Phe-Arg-MCA as the substrate. Cathepsin activity was approxymately 4-fold higher in the SF of RA patients than in those of patients with osteoarthritis. Cathepsin B and cathepsin L were separated by cation-exchange column chromatography. As a result, a large peak corresponding to cathepsin B and a very small peak correponding to cathepsin L were detected.
Biochemical sequential fractionation of the cathepsin purified from the SF showed that the large peak was mainly composed of cathepsin B. This purified enzyme induced conversion of pro-urokinase to urokinase, and the Km for pro-urokinase was approximately 8.27μM.
These findings indicated that an imbalance between cathepsin B and its inhibitors occurred due to increased concentrations of active cathepsin B in RA articular lesions, and that cathepsin B might be related to the degradation of cartilage in RA by activating the fibrinolytic cascade.
Journal Title
The journal of medical investigation : JMI
ISSN
13431420
NCID
AA11166929
Volume
47
Issue
1-2
Start Page
61
End Page
75
Sort Key
61
Published Date
2000
Remark
EDB ID
FullText File
language
eng