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Hydroquinone, a cigarette smoke compound, affects cartilage homeostasis through activation of the aryl hydrocarbon receptor pathway

Cintia Scucuglia Heluany, Anna de Palma, Nicholas Day, Sandra Helena Poliselli Farsky, Giovana Nalesso
doi: https://doi.org/10.1101/2022.04.25.489372
Cintia Scucuglia Heluany
1Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of São Paulo, São Paulo, Brazil
2Department of Pre-Clinical Sciences, School of Veterinary Medicine, University of Surrey, Guildford, UK
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Anna de Palma
2Department of Pre-Clinical Sciences, School of Veterinary Medicine, University of Surrey, Guildford, UK
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Nicholas Day
2Department of Pre-Clinical Sciences, School of Veterinary Medicine, University of Surrey, Guildford, UK
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Sandra Helena Poliselli Farsky
1Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of São Paulo, São Paulo, Brazil
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Giovana Nalesso
2Department of Pre-Clinical Sciences, School of Veterinary Medicine, University of Surrey, Guildford, UK
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  • For correspondence: g.nalesso@surrey.ac.uk
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Abstract

Exposure to cigarette smoke has a proven detrimental impact on different aspects of human health. Increasing evidences link smoking to degeneration of joint tissues. However, the toxic mechanisms elicited by the different components of cigarette smoke have not been fully elucidated yet. We have previously shown that exposure to hydroquinone (HQ), a pro-oxidant chemical present in cigarette smoke, can promote joint tissue degradation in murine models of rheumatoid arthritis through the activation of the aryl hydrocarbon receptor (AhR) pathway. Osteoarthritis (OA) is a chronic debilitating articular disease characterized by progressive degradation of the articular cartilage, whose onset and progression have also been associated with smoking. In this work we aimed to investigate the effect of HQ exposure on articular chondrocytes and how it affects cartilage homeostasis. Cell viability, gene expression, oxidative stress and inflammatory parameters were quantified in primary articular chondrocytes exposed to HQ in presence or absence of IL-1β pre-stimulation. HQ stimulation downregulated phenotypic markers genes such as SOX-9 and Col2a1, whereas upregulated the expression of the catabolic enzymes MMP-3 and ADAMTS5. HQ also promoted oxidative stress and reduced proteoglycan content. HQ exacerbated the pro-inflammatory effects mediated by the IL-1β co-stimulation. Finally, we showed that HQ-degenerative effects were mediated by the activation of AhR. Together, our findings address the harmful effects of HQ in the articular cartilage health, providing novel evidence surrounding the toxic mechanisms of environmental pollutants underlying the onset of articular diseases.

Competing Interest Statement

The authors have declared no competing interest.

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Posted April 26, 2022.
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Hydroquinone, a cigarette smoke compound, affects cartilage homeostasis through activation of the aryl hydrocarbon receptor pathway
Cintia Scucuglia Heluany, Anna de Palma, Nicholas Day, Sandra Helena Poliselli Farsky, Giovana Nalesso
bioRxiv 2022.04.25.489372; doi: https://doi.org/10.1101/2022.04.25.489372
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Hydroquinone, a cigarette smoke compound, affects cartilage homeostasis through activation of the aryl hydrocarbon receptor pathway
Cintia Scucuglia Heluany, Anna de Palma, Nicholas Day, Sandra Helena Poliselli Farsky, Giovana Nalesso
bioRxiv 2022.04.25.489372; doi: https://doi.org/10.1101/2022.04.25.489372

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