Circulating healing (CH) cells expressing BST2 are functionally activated by the injury-regulated systemic factor HGFA.
Circulating healing (CH) cells expressing BST2 are functionally activated by the injury-regulated systemic factor HGFA.
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DOI：
10.1186/s13287-018-1056-1
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发表时间：
2018-11-08
影响因子：
7.5
通讯作者：
Tasso R
中科院分区：
文献类型：
--
作者：
Lo Sicco C;Reverberi D;Villa F;Pfeffer U;Quarto R;Cancedda R;Tasso R
通过激活内源性祖细胞恢复受损组织是一种有吸引力的治疗选择。深入评价干/祖细胞的内在特性以及与受损环境的相互作用至关重要。在这里，我们表明骨髓基质细胞抗原2（BST 2）可以分离循环祖细胞群体，即循环愈合（CH）细胞，其特征在于独特的核心特征。BST 2 pos CH细胞的骨髓（BM）来源已通过瘦素受体的共表达而得到加强，瘦素受体是BM-骨骼干细胞亚群的标志。BST 2 pos CH细胞保留了以下能力：（i）对骨折产生的损伤信号做出反应，（ii）在损伤后改变细胞运动基因的表达，以及（iii）对肝细胞生长因子激活因子（HGFA）做出反应，HGFA是一种损伤相关刺激，足以诱导其转变为GALERT，即细胞功能性激活并参与组织修复的状态。总之，这些结果可以为识别新的策略铺平道路，以增强和加强未来治疗的内源性再生机制。本文的在线版本（10.1186/s13287-018-1056-1）包含补充材料，可供授权用户使用。
Restoration of damaged tissues through the activation of endogenous progenitors is an attractive therapeutic option. A deep evaluation of the intrinsic stem/progenitor cell properties as well as the reciprocal interactions with injured environments is of critical importance. Here, we show that bone marrow stromal cell antigen 2 (BST2) allows the isolation of a population of circulating progenitors, the circulating healing (CH) cells, characterized by a distinctive core signature. The bone marrow (BM) origin of BST2pos CH cells has been strengthened by the co-expression of leptin receptor, the hallmark of a subpopulation of BM-skeletal stem cells. BST2pos CH cells retained the capacity to (i) respond to injury signals generated by a bone fracture, (ii) modify the expression of cell motility genes following damage, and (iii) react to hepatocyte growth factor-activator (HGFA), an injury-related stimulus sufficient to induce their transition into GALERT, a state in which cells are functionally activated and participate in tissue repair. Taken together, these results could pave the way for the identification of new strategies to enhance and potentiate endogenous regenerative mechanisms for future therapies. The online version of this article (10.1186/s13287-018-1056-1) contains supplementary material, which is available to authorized users.
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影响因子：
4.4
作者：
Roson-Burgo B;Sanchez-Guijo F;Del Cañizo C;De Las Rivas J
通讯作者：
De Las Rivas J
DOI：
10.1126/science.1180794
发表时间：
2010-01-29
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Li L;Clevers H
通讯作者：
Clevers H
影响因子：
8.8
作者：
Rodgers, Joseph T.;Schroeder, Matthew D.;Rando, Thomas A.
通讯作者：
Rando, Thomas A.
DOI：
10.1158/1078-0432.ccr-10-1499
发表时间：
2011-08-01
期刊：
Clinical cancer research : an official journal of the American Association for Cancer Research
影响因子：
--
作者：
Li L;Bhatia R
通讯作者：
Bhatia R
影响因子：
4.6
作者：
Dotsenko, Olena;Xiao, Qingzhong;Jahangiri, Marjan
通讯作者：
Jahangiri, Marjan