Increased Wnt/β-catenin signaling contributes to autophagy inhibition resulting from a dietary magnesium deficiency in injury-induced osteoarthritis

• DOI: 10.1186/s13075-022-02848-0
• Publication Date: 2022-07-08T07:03:33Z
• Authors: Ruijun Bai; Michael Z. Miao; Hui Li; Yiqing Wang; Ruixue Hou; Ke He; Xuan Wu; Hongyu Jin; Chao Zeng; Yang Cui; Guanghua Lei
• Keywords: Magnesium deficiency (plants)

Abstract Background Dietary magnesium deficiency, which is common in modern diet, has been associated with osteoarthritis (OA) susceptibility. Despite this clinical association, no study addressed if dietary deficiency accelerates OA development, especially at molecular level. This aimed to explore aggravating effects of on cartilage damage an injury-induced murine model and determine the underlying mechanism. Methods Twelve-week-old C57BL/6J mice subject modeling were randomized into different diet groups fed a daily recommended content (500 mg/kg) or diets low (100 300 mg/kg). Articular was evaluated using OARSI score. To mechanisms vitro, mouse chondrocytes treated media conditions 0.1 0.4 mM, compared normal condition 0.7 mM as control. Anabolic catabolic factors, autophagy markers, β-catenin, Wnt ligands, channel transient receptor potential cation subfamily member 7 (TRPM7) analyzed by quantitative real-time PCR immunoblotting. Autolysosomes detected DALGreen staining via fluorescence microscopy autophagosomes transmission electron microscopy. Autophagy TRPM7 assessed vivo cartilage, comparing between immunohistochemistry. Results aggravated damage, indicated significant higher scores. markers LC3-II Beclin-1 decreased both diet-fed magnesium-treated chondrocytes. The number autolysosomes also reduced under conditions. Moreover, induced anabolic increased effect could be restored activator rapamycin. In addition, mediated activated Wnt/β-catenin signaling. expression mice, indicating that downstream changes regulated through channel. Conclusions contributes signaling activation. These findings benefits adequate for patients those individuals high risk OA.