Peng Hui, Guo Qi, Xiao Ye, Su Tian, Jiang Tie-Jian, Guo Li-Juan, Wang Min
Department of Endocrinology, Endocrinology Research Center, Xiangya Hospital of Central South University, Changsha, China.
Front Cell Dev Biol. 2020 Sep 3;8:872. doi: 10.3389/fcell.2020.00872. eCollection 2020.
Osteogenesis and senescence of BMSCs play great roles in age-related bone loss. However, the causes of these dysfunctions remain unclear. In this study, we identified a differentially expressed gene in middle-aged and elderly aged groups which were obtained from GSE35955. Subsequent analysis in various databases, such as TCGA, GTEx, and CCLE, revealed that had positive correlations with several osteogenic markers. The depletion of mouse suppressed the capacity of osteogenic differentiation in bone marrow mesenchymal stem cells (BMSCs). Notably, the expression of decreased during aging and senescence. The deficiency of accelerated cellular senescence in BMSCs. Conversely, the overexpression of enhanced the capacity of osteogenic differentiation and inhibited cellular senescence. Mechanistically, regulated Wnt signaling mediated by Gsk3β. Taken together, our data established that was potentially involved in the pathogenesis of age-related bone loss through regulating cellular senescence and osteogenic differentiation, which provides some new insights to treat age-related bone loss.
骨髓间充质干细胞（BMSCs）的成骨作用和衰老在与年龄相关的骨质流失中起重要作用。然而，这些功能障碍的原因仍不清楚。在本研究中，我们从GSE35955中鉴定出中年和老年组中差异表达的基因。随后在各种数据库（如TCGA、GTEx和CCLE）中的分析表明，该基因与几种成骨标志物呈正相关。小鼠该基因的缺失抑制了骨髓间充质干细胞（BMSCs）的成骨分化能力。值得注意的是，该基因的表达在衰老过程中降低。该基因的缺乏加速了BMSCs的细胞衰老。相反，该基因的过表达增强了成骨分化能力并抑制了细胞衰老。机制上，该基因通过Gsk3β调节Wnt信号通路。综上所述，我们的数据表明该基因可能通过调节细胞衰老和成骨分化参与与年龄相关的骨质流失的发病机制，这为治疗与年龄相关的骨质流失提供了一些新的见解。
