Expression of novel extracellular sulfatases Sulf-1 and Sulf-2 in normal and osteoarthritic articular cartilage.docVIP
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Expression of novel extracellular sulfatases Sulf-1 and Sulf-2 in normal and osteoarthritic articular cartilage
Available online /content/10/3/R61
Research article
Open Access
Vol 10 No 3
Expression of novel extracellular sulfatases Sulf-1 and Sulf-2 in
normal and osteoarthritic articular cartilage
Shuhei Otsuki1, Noboru Taniguchi1, Shawn P Grogan1, Darryl DLima1, Mitsuo Kinoshita2 and
Martin Lotz1
1Division of Arthritis Research, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA
2Department of Orthopedic Surgery, Osaka Medical College, 2–7 Daigaku-machi Takatsuki 569-8686, Osaka, Japan
Corresponding author: Shuhei Otsuki, otsuki@
Received: 14 Jan 2008 Revisions requested: 18 Feb 2008 Revisions received: 4 Apr 2008 Accepted: 28 May 2008 Published: 28 May 2008
Arthritis Research Therapy 2008, 10:R61 (doi:10.1186/ar2432)
This article is online at: /content/10/3/R61
? 2008 Otsuki et al.; licensee BioMed Central Ltd.
This is an open access article distributed under the terms of the Creative Commons Attribution License (/licenses/by/2.0),
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Introduction
Changes
in
sulfation
of
cartilage
2 mRNA expression as compared with normal human articular
cartilage. Sulf protein expression in OA cartilage was prominent
in the cell clusters. Western blotting revealed a profound
increase in Sulf protein levels in human OA cartilage. In normal
mouse joints, Sulf expression was similar to human cartilage,
and with increasing age, there was a marked upregulation of
Sulf.
glycosaminoglycans as mediated by sulfatases can regulate
growth factor signaling. The aim of this study was to analyze
expression patterns of recently identified extracellular sulfatases
Sulf-1 and Sulf-2 in articular cartilage and chondrocytes.
Methods Sulf-1 and Sulf-2 expressions in human articular
cartilage from normal donors and patients with osteoarthritis
(OA) and in normal and aged mouse joints were
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