Early and long-standing rheumatoid arthritis: distinct molecular signatures identified by gene-expression profiling in synovia
- Equal contributors
1 Department of Rheumatology, Rouen University Hospital and Inserm 905 & Institut Fédératif de Recherche Multidisciplinaire sur les Peptides 23, Institute for Biomedical Research, University of Rouen, 76031 Rouen Cedex, and Consortium EGERIE, France
2 Inserm Unité 905, Institut Fédératif de Recherche Multidisciplinaire sur les Peptides 23, Institute for Biomedical Research, University of Rouen, Faculté de Médecine-Pharmacie, Rouen, France
3 Department of Rheumatology, Cochin Hospital, AP-HP, University of Paris-Descartes, 27, rue du faubourg Saint-Jacques, 75679 Paris Cedex 14, France
4 Department of Orthopedic and Traumatology, Rouen University Hospital, 76031 Rouen Cedex, France
5 Department of Plastic and Reconstructive Surgery, Rouen University Hospital, 76031 Rouen Cedex, France
6 Institut Cochin, Université Paris Descartes, Inserm (U567), CNRS (UMR8104), Paris, and Consortium EGERIE, France
Citation and License
Arthritis Research & Therapy 2009, 11:R99 doi:10.1186/ar2744Published: 29 June 2009
Rheumatoid arthritis (RA) is a heterogeneous disease and its underlying molecular mechanisms are still poorly understood. Because previous microarray studies have only focused on long-standing (LS) RA compared to osteoarthritis, we aimed to compare the molecular profiles of early and LS RA versus control synovia.
Synovial biopsies were obtained by arthroscopy from 15 patients (4 early untreated RA, 4 treated LS RA and 7 controls, who had traumatic or mechanical lesions). Extracted mRNAs were used for large-scale gene-expression profiling. The different gene-expression combinations identified by comparison of profiles of early, LS RA and healthy synovia were linked to the biological processes involved in each situation.
Three combinations of 719, 116 and 52 transcripts discriminated, respectively, early from LS RA, and early or LS RA from healthy synovia. We identified several gene clusters and distinct molecular signatures specifically expressed during early or LS RA, thereby suggesting the involvement of different pathophysiological mechanisms during the course of RA.
Early and LS RA have distinct molecular signatures with different biological processes participating at different times during the course of the disease. These results suggest that better knowledge of the main biological processes involved at a given RA stage might help to choose the most appropriate treatment.