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PLoS Genet. 2005 Oct;1(4):e48. Epub 2005 Oct 28.

Cytoskeletal rearrangements in synovial fibroblasts as a novel pathophysiological determinant of modeled rheumatoid arthritis.

Author information

1
Institute of Immunology, Alexander Fleming Biomedical Sciences Research Center, Athens, Greece. V.Aidinis@Fleming.gr

Erratum in

  • PLoS Genet. 2005 Nov;1(5):e73. Kazunori, Waki [corrected to Waki, Kazunori].

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.

PMID:
16254600
PMCID:
PMC1270006
DOI:
10.1371/journal.pgen.0010048
[Indexed for MEDLINE]
Free PMC Article

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