Cytoskeletal rearrangements in synovial fibroblasts as a novel pathophysiological determinant of modeled rheumatoid arthritis.
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,...
| Main Authors: | , , , , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Public Library of Science (PLoS)
2005-10-01
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| Series: | PLoS Genetics |
| Online Access: | http://europepmc.org/articles/PMC1270006?pdf=render |
| _version_ | 1818418862329167872 |
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| author | Vassilis Aidinis Piero Carninci Maria Armaka Walter Witke Vaggelis Harokopos Norman Pavelka Dirk Koczan Christos Argyropoulos Maung-Maung Thwin Steffen Möller Kazunori Waki Ponnampalam Gopalakrishnakone Paola Ricciardi-Castagnoli Hans-Jürgen Thiesen Yoshihide Hayashizaki George Kollias |
| author_facet | Vassilis Aidinis Piero Carninci Maria Armaka Walter Witke Vaggelis Harokopos Norman Pavelka Dirk Koczan Christos Argyropoulos Maung-Maung Thwin Steffen Möller Kazunori Waki Ponnampalam Gopalakrishnakone Paola Ricciardi-Castagnoli Hans-Jürgen Thiesen Yoshihide Hayashizaki George Kollias |
| author_sort | Vassilis Aidinis |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-12-14T12:29:25Z |
| format | Article |
| id | doaj.art-10ed93b4fa424923994fb2a12790a29f |
| institution | Directory Open Access Journal |
| issn | 1553-7390 1553-7404 |
| language | English |
| last_indexed | 2024-12-14T12:29:25Z |
| publishDate | 2005-10-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS Genetics |
| spelling | doaj.art-10ed93b4fa424923994fb2a12790a29f2022-12-21T23:01:14ZengPublic Library of Science (PLoS)PLoS Genetics1553-73901553-74042005-10-0114e4810.1371/journal.pgen.0010048Cytoskeletal rearrangements in synovial fibroblasts as a novel pathophysiological determinant of modeled rheumatoid arthritis.Vassilis AidinisPiero CarninciMaria ArmakaWalter WitkeVaggelis HarokoposNorman PavelkaDirk KoczanChristos ArgyropoulosMaung-Maung ThwinSteffen MöllerKazunori WakiPonnampalam GopalakrishnakonePaola Ricciardi-CastagnoliHans-Jürgen ThiesenYoshihide HayashizakiGeorge KolliasRheumatoid 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.http://europepmc.org/articles/PMC1270006?pdf=render |
| spellingShingle | Vassilis Aidinis Piero Carninci Maria Armaka Walter Witke Vaggelis Harokopos Norman Pavelka Dirk Koczan Christos Argyropoulos Maung-Maung Thwin Steffen Möller Kazunori Waki Ponnampalam Gopalakrishnakone Paola Ricciardi-Castagnoli Hans-Jürgen Thiesen Yoshihide Hayashizaki George Kollias Cytoskeletal rearrangements in synovial fibroblasts as a novel pathophysiological determinant of modeled rheumatoid arthritis. PLoS Genetics |
| title | Cytoskeletal rearrangements in synovial fibroblasts as a novel pathophysiological determinant of modeled rheumatoid arthritis. |
| title_full | Cytoskeletal rearrangements in synovial fibroblasts as a novel pathophysiological determinant of modeled rheumatoid arthritis. |
| title_fullStr | Cytoskeletal rearrangements in synovial fibroblasts as a novel pathophysiological determinant of modeled rheumatoid arthritis. |
| title_full_unstemmed | Cytoskeletal rearrangements in synovial fibroblasts as a novel pathophysiological determinant of modeled rheumatoid arthritis. |
| title_short | Cytoskeletal rearrangements in synovial fibroblasts as a novel pathophysiological determinant of modeled rheumatoid arthritis. |
| title_sort | cytoskeletal rearrangements in synovial fibroblasts as a novel pathophysiological determinant of modeled rheumatoid arthritis |
| url | http://europepmc.org/articles/PMC1270006?pdf=render |
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