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Secretome analysis of human articular chondrocytes unravels catabolic effects of nicotine on the joint
Author(s) -
Lourido Lucía,
Calamia Valentina,
FernándezPuente Patricia,
Mateos Jesús,
Oreiro Natividad,
Blanco Francisco J.,
RuizRomero Cristina
Publication year - 2016
Publication title -
proteomics – clinical applications
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.948
H-Index - 54
eISSN - 1862-8354
pISSN - 1862-8346
DOI - 10.1002/prca.201400186
Subject(s) - nicotine , osteoarthritis , inflammation , cartilage , extracellular matrix , western blot , proteases , matrix metalloproteinase , catabolism , secretion , medicine , articular cartilage damage , chemistry , pharmacology , immunology , pathology , articular cartilage , biochemistry , anatomy , enzyme , alternative medicine , gene , metabolism
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.