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Abstract：
The pathological advancement of osteoporosis is caused by the uneven development of bone marrow-derived mesenchymal stem cells (BMSCs) in terms of osteogenesis and adipogenesis. While the role of EEF1B2 in intellectual disability and tumorigenesis is well established, its function in the bone-fat switch of BMSCs is still largely unexplored. During the process of osteogenic differentiation, we observed an increase in the expression of EEF1B2, while a decrease in its expression was noted during adipogenesis. Suppression of EEF1B2 hindered the process of osteogenic differentiation and mineralization while promoting adipogenic differentiation. On the contrary, overexpression of EEF1B2 enhanced osteogenesis and strongly inhibited adipogenesis. Furthermore, the excessive expression of EEF1B2 in the tibias has the potential to mitigate bone loss and decrease marrow adiposity in mice with osteoporosis. In terms of mechanism, the suppression of β-catenin activity occurred when EEF1B2 function was suppressed during osteogenesis. Our collective findings indicate that EEF1B2 functions as a regulator, influencing the differentiation of BMSCs and maintaining a balance between bone and fat. Our finding highlights its potential as a therapeutic target for diseases related to bone metabolism.
摘要：
骨质疏松症的病理进展是由骨髓间充质干细胞（BMSCs）在成骨和脂肪形成方面的不平衡发育引起的。虽然EEF1B2在智力障碍和肿瘤发生中的作用已经确立，其在BMSCs的骨-脂肪开关中的功能仍未被研究。在成骨分化的过程中，我们观察到EEF1B2的表达增加，而在脂肪形成期间其表达减少。EEF1B2的抑制阻碍了成骨分化和矿化的过程,同时促进成脂分化。相反,EEF1B2的过表达可增强成骨并强烈抑制脂肪生成。此外，EEF1B2在胫骨中的过度表达有可能减轻骨质疏松症小鼠的骨丢失和减少骨髓肥胖。在机制方面,当在成骨过程中EEF1B2功能受到抑制时，β-catenin活性受到抑制。我们的集体发现表明，EEF1B2作为一个调节器，影响BMSCs的分化，维持骨与脂肪的平衡。我们的发现强调了它作为骨代谢相关疾病的治疗靶点的潜力。
