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La consommation tabagique comme facteur de risque environnemental de l’arthrose : rôle de la nicotine dans la prolifération et la différenciation chondrogénique des cellules souches mésenchymateuses humaines

Abstract : Among the environmental risk factors for osteoarthritis (OA), tobacco consumption features prominently but is still controversial today. Among the 4,000 compounds present in cigarette smoke, nicotine is one of the most physiologically active molecules. The aim of the study is to measure the impact of nicotine on human chondrocytes and on the proliferation and chondrogenic differentiation of Wharton’s Jelly stem cells (WJ-MSC). We found that nicotine at the concentrations used had no effect on the proliferation of primary human OA chondrocytes, but induced an increase in the expression of matrix metalloproteases (MMP13). It unravels the catabolic effects of nicotine in the joint by stimulating matrix degradation. This result suggests a pro-catabolic effect of nicotine in the joint by stimulating matrix degradation. In smokers, the synthesis as well as the degradation pathways in chondrocytes are stimulated, when compared to no smokers. In addition, the cell proliferation and migration of WJ-MSC were significantly impaired by nicotine, and it also had an adverse effect on the chondrogenesis of WJ-MSC by stimulating the inflammatory response and hypertrophic differentiation. We have shown, for the first time, the expression of the nicotinic acetylcholine receptor (nAChR), in particular that of the α7 subunit in the WJ-MSC at the transcriptional and translational levels. The adverse effect of nicotine on WJ-MSC was probably mediated by α7 nAChR. Interestingly, α-Bungarotoxin (α-BTX), a specific inhibitor of α7 nAChR, could partially reverse this effect. In conclusion the results show that nicotine has an adverse effect on the ontogenesis of cartilage, and potentially induces an increase in the prevalence of osteoarthritis in adults
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  • HAL Id : tel-01684227, version 1

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Xu Yang. La consommation tabagique comme facteur de risque environnemental de l’arthrose : rôle de la nicotine dans la prolifération et la différenciation chondrogénique des cellules souches mésenchymateuses humaines. Médecine humaine et pathologie. Université de Lorraine, 2017. Français. ⟨NNT : 2017LORR0050⟩. ⟨tel-01684227⟩

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