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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Aged, Aged, 80 and over, Cartilage, Articular, Case-Control Studies, Chitinase-3-Like Protein 1, Chondrocytes, Extracellular Matrix, Female, Fibronectins, Gene Expression Profiling, Gene Expression Regulation, Humans, Interleukin-1beta, Male, Matrix Metalloproteinase 1, Metabolism, Models, Biological, Nicotine, Osteoarthritis, Primary Cell Culture, Smoking.
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Does secretome analysis of human articular chondrocytes unravel catabolic effects of nicotine on the joint? Context: 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. 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. 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.
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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. Final Decision: yes