Synovial Fibroblasts (SFs) are unique mesenchymal cells populating the synovium, a membrane that defines diarthroses. Under normal conditions, SFs assure the structural and dynamic integrity of synovial joints by coordinating the composition of the synovial fluid and the extracellular matrix of the joint lining. In arthritic diseases however, SFs revert themselves from a homeostatic regulator to a pathogenic orchestrator by increasing in number and regulating the destruction of joint architecture. Whether the excess of SFs originates mostly from a discrepancy in their physiological regenerative capacity or the increased differentiation and migration of mesenchymal stem cells and other cells could also contribute, still remains obscure. It has been previously shown that rheumatoid SFs are resistant to apoptosis in vitro, they maintain their inflammatory memory ex vivo, and they transfer disease when implanted orthotopically in healthy joints, suggesting that their abnormalities are imprinted and persist even upon their removal from the cytokine and growth factor milieu of the disease-affected synovium.
Our group is dedicated in understanding the molecular identity of synovial fibroblasts (SFs) and its impact in the development and perpetuation of inflammatory arthritic diseases following functional genetic and genomic approaches. To achieve our mission, our group works towards two directions:
1. The characterization and the functional significance of the mesenchymal cell subpopulations of synovium under normal and chronic arthritic diseases
2. The identification of pathways and druggable molecular determinants which will cease the SF pathogenic autonomy