Potential involvement of oxidative stress in cartilage senescence and development of osteoarthritis oxidative stress induces chondrocyte telomere instability and downregulation of chondrocyte function 英文参考文献.docVIP
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Potential involvement of oxidative stress in cartilage senescence and development of osteoarthritis oxidative stress induces chondrocyte telomere instability and downregulation of chondrocyte function 英文参考文献
Available online /content/7/2/R380
Research article
Open Access
Vol 7 No 2
Potential involvement of oxidative stress in cartilage senescence
and development of osteoarthritis: oxidative stress induces
chondrocyte telomere instability and downregulation of
chondrocyte function
Kazuo Yudoh, Nguyen van Trieu, Hiroshi Nakamura, Kayo Hongo-Masuko, Tomohiro Kato and
Kusuki Nishioka
Department of Bioregulation, Institute of Medical Science, St. Marianna University, Kawasaki City, Japan
Corresponding author: Kazuo Yudoh, yudo@marianna-u.ac.jp
Received: 13 Nov 2003 Revisions requested: 4 Dec 2003 Revisions received: 25 Nov 2004 Accepted: 10 Dec 2004 Published: 26 Jan 2005
Arthritis Res Ther 2005, 7:R380-R391 (DOI 10.1186/ar1499)
? 2005 Yudoh et al.; licensee BioMed Central Ltd.
/content/7/2/R380
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
Oxidative stress leads to increased risk for osteoarthritis (OA)
but the precise mechanism remains unclear. We undertook this
study to clarify the impact of oxidative stress on the progression
of OA from the viewpoint of oxygen free radical induced
genomic instability, including telomere instability and resulting
replicative senescence and dysfunction in human chondrocytes.
Human chondrocytes and articular cartilage explants were
isolated from knee joints of patients undergoing arthroplastic
knee surgery for OA. Oxidative damage and antioxidative
capacity in OA cartilage were investigated in donor-matched
pairs of intact and degenerated regions of tissue isolated from
the same cartilage explants. The results were histologically
confirmed by immunohistochemistry for nitrotyrosine, which is
considered to be a maker of oxidative damage. Under treatment
with reactive oxyg
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