Lucía Lourido1, Valentina Calamia1, Patricia Fernández-Puente1, Jesús Mateos1, Natividad Oreiro1, Francisco J Blanco1,2, Cristina Ruiz-Romero1,3. 1. Proteomics Group-PBR2-ProteoRed/ISCIII, Rheumatology Division, Instituto de Investigación Biomédica de A Coruña (INIBIC), Complexo Hospitalario Universitario de A Coruña (CHUAC), Sergas, Universidade da Coruña (UDC), A Coruña, Spain. 2. RIER-RED de Inflamación y Enfermedades Reumáticas, Instituto de Investigación Biomédica de A Coruña (INIBIC), Complexo Hospitalario Universitario de A Coruña (CHUAC), A Coruña, Spain. 3. CIBER-BBN Instituto de Salud Carlos III, Instituto de Investigación Biomédica de A Coruña (INIBIC), Complexo Hospitalario Universitario de A Coruña (CHUAC), A Coruña, Spain.
Abstract
PURPOSE: Osteoarthritis (OA) is a degenerative joint pathology characterized by articular cartilage degradation that lacks from efficient therapy. Since previous epidemiological data show a high controversy regarding the role of smoking in OA, we aimed to evaluate the effects of nicotine (the most physiologically active compound of tobacco) on the joint. EXPERIMENTAL DESIGN: Secretome analyses, based on metabolic labeling followed by LC-MALDI-TOF/TOF analysis, were carried out using an in vitro model of articular inflammation (primary human articular chondrocytes treated with interleukin-1β), and also on osteoarthritic cells. ELISA and Western blot assays were performed to verify some of the results. RESULTS: Nineteen proteins were altered by nicotine in the model of articular inflammation, including several cytokines and proteases. We confirmed the increased secretion by nicotine of matrix metalloproteinase 1 and two proposed markers of OA, fibronectin, and chitinase 3-like protein 1. Finally, four components of the extracellular matrix of cartilage were decreased by nicotine in OA chondrocytes. CONCLUSIONS AND CLINICAL RELEVANCE: Our data contribute to a better understanding of the molecular mechanisms that are modulated by nicotine in cartilage cells, suggesting a negative effect of this drug on the joint.
PURPOSE:Osteoarthritis (OA) is a degenerative joint pathology characterized by articular cartilage degradation that lacks from efficient therapy. Since previous epidemiological data show a high controversy regarding the role of smoking in OA, we aimed to evaluate the effects of nicotine (the most physiologically active compound of tobacco) on the joint. EXPERIMENTAL DESIGN: Secretome analyses, based on metabolic labeling followed by LC-MALDI-TOF/TOF analysis, were carried out using an in vitro model of articular inflammation (primary human articular chondrocytes treated with interleukin-1β), and also on osteoarthritic cells. ELISA and Western blot assays were performed to verify some of the results. RESULTS: Nineteen proteins were altered by nicotine in the model of articular inflammation, including several cytokines and proteases. We confirmed the increased secretion by nicotine of matrix metalloproteinase 1 and two proposed markers of OA, fibronectin, and chitinase 3-like protein 1. Finally, four components of the extracellular matrix of cartilage were decreased by nicotine in OA chondrocytes. CONCLUSIONS AND CLINICAL RELEVANCE: Our data contribute to a better understanding of the molecular mechanisms that are modulated by nicotine in cartilage cells, suggesting a negative effect of this drug on the joint.
Authors: Antonietta Stellavato; Valentina Vassallo; Annalisa La Gatta; Anna Virginia Adriana Pirozzi; Mario De Rosa; Giovanni Balato; Alessio D'Addona; Virginia Tirino; Carlo Ruosi; Chiara Schiraldi Journal: Biomed Res Int Date: 2019-04-23 Impact factor: 3.411
Authors: Ana Belen Rivas; Amanda Lopez-Picado; Valentina Calamia; Ester Carreño; Lidia Cocho; Miguel Cordero-Coma; Alex Fonollosa; Felix M Francisco Hernandez; Angel Garcia-Aparicio; Javier Garcia-Gonzalez; Jose Juan Mondejar; Leticia Lojo-Oliveira; Llucí Martínez-Costa; Santiago Munoz; Diana Peiteado; Jose Antonio Pinto; Beatriz Rodriguez-Lozano; Esperanza Pato; David Diaz-Valle; Elena Molina; Luis Alberto Tebar; Luis Rodriguez-Rodriguez Journal: BMJ Open Date: 2022-03-22 Impact factor: 2.692