Open AccessComparative analysis of gene expression profiles in intact and damaged regions of human osteoarthritic cartilage
Author(s) -
Sato Tomoo,
Konomi Koji,
Yamasaki Satoshi,
Aratani Satoko,
Tsuchimochi Kaneyuki,
Yokouchi Masahiro,
MasukoHongo Kayo,
Yagishita Naoko,
Nakamura Hiroshi,
Komiya Setsuro,
Beppu Moroe,
Aoki Haruhito,
Nishioka Kusuki,
Nakajima Toshihiro
Publication year - 2006
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/art.21638
Subject(s) - cartilage , osteoarthritis , gene expression , gene , microarray analysis techniques , real time polymerase chain reaction , messenger rna , microbiology and biotechnology , microarray , biology , reverse transcription polymerase chain reaction , pathology , genetics , anatomy , medicine , alternative medicine
Objective To analyze the differences in gene expression profiles of chondrocytes in intact and damaged regions of cartilage from the same knee joint of patients with osteoarthritis (OA) of the knee. Methods We compared messenger RNA expression profiles in regions of intact and damaged cartilage (classified according to the Mankin scale) obtained from patients with knee OA. Five pairs of intact and damaged regions of OA cartilage were evaluated by oligonucleotide array analysis using a double in vitro transcription amplification technique. The microarray data were confirmed by real‐time quantitative polymerase chain reaction (PCR) amplification and were compared with previously published data. Results About 1,500 transcripts, which corresponded to 8% of the expressed transcripts, showed ≥2‐fold differences in expression between the cartilage tissue pairs. Approximately 10% of these transcripts (n = 151) were commonly expressed in the 5 patient samples. Accordingly, 114 genes (35 genes expressed in intact > damaged; 79 genes expressed in intact < damaged) were selected. The expression of some genes related to the wound‐healing process, including cell proliferation and interstitial collagen synthesis, was higher in damaged regions than in intact regions, similar to the findings for genes that inhibit matrix degradation. Comparisons of the real‐time quantitative PCR data with the previously reported data support the validity of our microarray data. Conclusion Differences between intact and damaged regions of OA cartilage exhibited a similar pattern among the 5 patients examined, indicating the presence of common mechanisms that contribute to cartilage destruction. Elucidation of this mechanism is important for the development of effective treatments for OA.