Pérez García, SeleneCalamia, ValentinaHermida-Gómez, TamaraGutiérrez Cañas, IreneCarrión Caballo, MarVillanueva Romero, RaúlCastro Vázquez, DavidMartínez Mora, María Del CarmenJuarranz Moratilla, YasminaBlanco, Francisco J.Pérez Gomáriz, Rosa María2023-06-172023-06-172021-06-161661-6596, ESSN: 1422-006710.3390/ijms22126441https://hdl.handle.net/20.500.14352/8694Osteoarthritis (OA) is the most common musculoskeletal disorder causing a great disability and a reduction in the quality of life. In OA, articular chondrocytes (AC) and synovial fibroblasts (SF) release innate-derived immune mediators that initiate and perpetuate inflammation, inducing cartilage extracellular matrix (ECM) degradation. Given the lack of therapies for the treatment of OA, in this study, we explore biomarkers that enable the development of new therapeutical approaches. We analyze the set of secreted proteins in AC and SF co-cultures by stable isotope labeling with amino acids (SILAC). We describe, for the first time, 115 proteins detected in SF-AC co-cultures stimulated by fibronectin fragments (Fn-fs). We also study the role of the vasoactive intestinal peptide (VIP) in this secretome, providing new proteins involved in the main events of OA, confirmed by ELISA and multiplex analyses. VIP decreases proteins involved in the inflammatory process (CHI3L1, PTX3), complement activation (C1r, C3), and cartilage ECM degradation (DCN, CTSB and MMP2), key events in the initiation and progression of OA. Our results support the anti-inflammatory and anti-catabolic properties of VIP in rheumatic diseases and provide potential new targets for OA treatment.engAtribución 3.0 Españahttps://creativecommons.org/licenses/by/3.0/es/Proteomic analysis of synovial fibroblasts and articular chondrocytes co-cultures reveals valuable VIP-modulated inflammatory and degradative proteins in osteoarthritisjournal articlehttps://doi.org/10.3390/ijms22126441https://www.mdpi.com/1422-0067/22/12/6441open access577.175.82616.72-022.77OsteoarthritisSynovial fibroblastsChondrocytesVIPCHI3L1PTX3Complement systemDecorinCathepsin BMMP2Bioquímica (Medicina)InmunologíaReumatología2412 Inmunología3205.09 Reumatología