Published in
Public Library of Science, PLoS Genetics, 5(1), p. e73, 2005
DOI: 10.1371/journal.pgen.0010073
Public Library of Science, PLoS Genetics, 4(1), p. e48, 2005
DOI: 10.1371/journal.pgen.0010048
Links
- ORCID
- Public Library of Science
- Public Library of Science
- [www.ncbi.nlm.nih.gov] | PDF
- [scholarbank.nus.edu.sg]
- [doaj.org] | PDF
- [doaj.org] | PDF
- [www.ncbi.nlm.nih.gov] | PDF
- [europepmc.org] | PDF
- [europepmc.org] | PDF
- [www.researchgate.net] | PDF
- [www.ncbi.nlm.nih.gov] | PDF
- [www.ncbi.nlm.nih.gov] | PDF
- [www.ncbi.nlm.nih.gov] | PDF
Tools
Cytoskeletal rearrangements in synovial fibroblasts as a novel pathophysiological determinant of modeled rheumatoid arthritis.
,
Walter Witke,
Vaggelis Harokopos,
Norman Pavelka,
Dirk Koczan,
Christos Argyropoulos,
Maung Thwin,
Steffen Möller,
Waki Kazunori,
Ponnampalam Gopalakrishnakone,
Paola Ricciardi-Castagnoli,
Hans-Jürgen Thiesen,
Yoshihide Hayashizaki
and other authors.
Full text: Download
Abstract
Rheumatoid arthritis is a chronic inflammatory disease with a high prevalence and substantial socioeconomic burden. Despite intense research efforts, its aetiology and pathogenesis remain poorly understood. To identify novel genes and/or cellular pathways involved in the pathogenesis of the disease, we utilized a well-recognized tumour necrosis factor-driven animal model of this disease and performed high-throughput expression profiling with subtractive cDNA libraries and oligonucleotide microarray hybridizations, coupled with independent statistical analysis. This twin approach was validated by a number of different methods in other animal models of arthritis as well as in human patient samples, thus creating a unique list of disease modifiers of potential therapeutic value. Importantly, and through the integration of genetic linkage analysis and Gene Ontology–assisted functional discovery, we identified the gelsolin-driven synovial fibroblast cytoskeletal rearrangements as a novel pathophysiological determinant of the disease.