目的：探讨核基质蛋白特异AT序列结合蛋白2（special AT-rich sequence-binding protein 2,SATB2）及相关分子在不同年龄段女性颌骨来源骨髓基质细胞（bone marrow stromal cells,BMSCs）中的表达,及其与BMSCs衰老表型的关系。方法：在患者知情同意前提下,获得因多生牙拔除或牙齿种植的年轻组、中年组和老年组女性下颌骨松质骨,贴壁培养法获得BMSCs;MTT检测细胞增殖能力;衰老染色检测细胞衰老,Western blot检测SATB2及NANOG、OCT4、SOX2等干细胞多潜能因子及衰老相关蛋白P16、P21、P53的表达;采用SATB2过表达病毒载体转染老年BMSCs,并分析其对BMSCs干性及衰老表型的影响。结果：颌骨BMSCs随着增龄性变化,其增殖活性逐渐降低,并呈现相应的衰老表型,核基质蛋白SATB2及多潜能转录因子表达逐渐下调;SATB2及多潜能因子与BMSCs体外复制性衰老及衰老信号哺乳动物雷帕霉素靶蛋白（mammalian target of rapam-ycin,m TOR）通路关系密切;老年BMSCs过表达SATB2后,干性指标表达升高,衰老染色阳性细胞数减少,m TOR、P-m TOR及衰老相关蛋白表达降低。结论：女性颌骨BMSCs呈现增龄性衰老特征,SATB2可能通过调节干细胞多潜能因子、抑制m TOR衰老信号通路,增强BMSCs的抗衰老能力。
Objective： The aim of this study was to investigate the expression of nuclear matrix proteins special AT-rich sequencebinding protein 2（ SATB2） and associated molecules in female mandible-derived bone marrow stromal cells（ BMSCs） taken from subjects at different ages,and their relationship with senescence phenotypes of BMSCs. Methods： Trabecular bones of female mandible were isolated from volunteers who sought treatment of impacted tooth or tooth implantation and divided into Y group,M group and O group. MTT and β-Gal staining were performed for analysis of cell proliferation and senescence,Western blot was used to examine the expression of SATB2,stemness factors and senescence-associated proteins. The effects of SATB2 on BMSCs stemness and senescence phenotypes were analyzed by overexpressed SATB2. Results： The proliferation ability,SATB2 and stemness factors expressions of BMSCs decreased with aging,meanwhile,showing increasing senescence phenotypes. SATB2 and stemness factors were closely associated with replicative senescence of BMSCs and mammalian target of rapamycin（ m TOR） signaling. After overexpression SATB2 in older BMSCs,the number of senescence positive cells and expression of stemness factors increased,but expression of m TOR,P-m TOR and senescence associated proteins decreased. Conclusions： Senescence of female mandible-derived BMSCs increased with aging. SATB2 may improve anti-senescence ability of BMSCs by regulating stemness factors and inhibiting m TOR signaling.