中文摘要：

以前的研究揭示了那根骨头从病人们早展出了的全身的豺狼座 erythematosus (SLE ) 的髓间充质的干细胞(BM-MSCs ) 老朽签名，它可以参予 SLE 的发展。然而，关于这现象的分子的机制充分没被阐明。在当前的学习，我们试图调查表明发信号的抄写(STAT ) 的变换器和使活跃之物的 Janus kinase (JAK ) 是否调停了从 SLE 病人的 BM-MSCs 的老朽。12 个女 SLE 病人和健康题目在学习被注册。所有 BM-MSCs 被密度坡度 centrifugation 孤立。西方的污点分析被用来测试表明分子的 JAK-STAT 的表示。我们由流动 cytometry 观察了房间，由染色的 F 肌动朊的细胞骨架结构的变化，和房间周期的分发的女郎的活动。从 SLE 病人的 BM-MSCs 显示出表明 transduction， phosphorylated JAK2 的高水平，和 STAT3 的 JAK-STAT 的老朽，和反常激活的突出的特征。在在正常 MSC 的 IFN- 的刺激以后，发信号的 JAK-STAT 被激活。房间体积和联系老朽的牛乳糖的数字(SA -- 女郎) 在 SLE BM-MSCs 积极被增加。细胞骨架的组织是将近混乱的。房间增长的率被减少。AG490， JAK2 的禁止者，并且在 BM-MSCs 的 STAT3 击倒，能显著地颠倒老朽。在摘要，我们的学习显示 JAK-STAT 发信号小径可以在 SLE BM-MSCs 的老朽起一个关键作用。

英文摘要：

Previous studies have revealed that bone marrow-mesenchymal stem cells （BM-MSCs） from systemic lupus erythematosus （SLE） patients exhibited early signs of senescence, which may participate in the development of SLE. However, the molecular mechanisms about this phenomenon have not been fully elucidated. In the current study, we aimed to investigate whether Janus kinase （JAK）-signaling transducers and activators of transcription （STAT） signaling mediated the senescence of BM-MSCs from SLE patients. Twelve female SLE patients and healthy subjects were enrolled in the study. All BM-MSCs were isolated by density gradient centdfugation. Western blot analysis was used to test the expression of JAK-STAT signaling molecules. We observed the activity of β-gal of cells, the changes of cytoskeletal structure by F-actin staining, and the distribution of cell cycle by flow cytometry. BM-MSCs from SLE patients showed prominent features of senescence, and abnormal activation of JAK-STAT sig- naling transduction, high level of phosphorylated JAK2, and STAT3. After stimulation of IFN-γ, in normal MSCs, JAK-STAT signaling was activated. The cell volume and the number of senescence-associated β-galactosidase （SA-β-gal） positive in SLE BM-MSCs were increased. The organization of cytoskeleton was nearly disordered. The rate of cell proliferation was decreased. AG490, the inhibitor of JAK2, and knockdown of STAT3 in BM-MSCs, could significantly reverse the senescence. In summary, our study indicated that JAK-STAT signaling pathway may play a critical role in the senescence of SLE BM-MSCs.