Children's Hospital, Boston, United States.
Matrix Biol. 2010 Oct;29(8):657-63. doi: 10.1016/j.matbio.2010.08.008. Epub 2010 Sep 7.
The goal of the present study was to devise an in vitro model suitable for investigations of the homing of mesenchymal stem cells to sites of injury. Such a model was designed on the basis of a "transwell" assay, with an insert seeded with human bone marrow stromal cells and a well with a desired cell type. To mimic physiological environment and to simulate "injury", cells in a well were maintained not only on tissue culture plastic but also on collagens I and IV, major matrix components in musculoskeletal and adipose tissues respectively, and subjected to a severe thermal stress. The results obtained showed a massive translocation of bone marrow stromal cells through the inserts' membrane toward the "injury" site. Unexpectedly, it emerged that collagen matrix is essential in producing such a migration. The results obtained suggest that upon injury cells secrete a substance which interacts with collagen matrix to produce a homing agent. The substance in question appears to be a protease and its interaction with the collagen matrix appears to be a digestion of the latter into fragments shown to be chemotactic. Both AEBSF, an inhibitor of serine proteases, and leupeptin, an inhibitor of cysteine proteases as well as of trypsin-like serine proteases, but not the broad spectrum MMP inhibitor marimastat, significantly inhibit the observed homing effect and this inhibition is not due to cytotoxicity. Moreover, immunoprecipitation of HTRA1, a trypsin-like serine protease known to be secreted by cells differentiating into all three major mesenchymal lineages and by stressed cells in general and shown to degrade a number of matrix proteins including collagen, significantly diminished the homing effect. The data suggest that this protease is a major contributor to the observed chemotaxis of bone marrow stromal cells. The present study indicates that collagen fragments can mediate the migration of bone marrow stromal cells. The results also suggest that, at least in musculoskeletal and in adipose tissues, matrix remodeling occurrences, usually closely associated with tissue remodeling, should also be regarded as potential stem cells recruitment events.
本研究的目的是设计一种适合研究间充质干细胞归巢到损伤部位的体外模型。这种模型是基于“transwell”测定法设计的,其中插入物中接种了人骨髓基质细胞,孔中培养了所需的细胞类型。为了模拟生理环境并模拟“损伤”,孔中的细胞不仅在组织培养塑料上,而且在胶原蛋白 I 和 IV 上维持,这分别是肌肉骨骼和脂肪组织中的主要基质成分,并受到严重的热应激。结果表明,大量骨髓基质细胞通过插入物的膜向“损伤”部位大量迁移。出乎意料的是,胶原蛋白基质在产生这种迁移中是必不可少的。结果表明,在损伤时,细胞分泌一种与胶原蛋白基质相互作用的物质,产生归巢因子。所涉及的物质似乎是一种蛋白酶,其与胶原蛋白基质的相互作用似乎是将后者消化成具有趋化性的片段。AEBSF,丝氨酸蛋白酶抑制剂,亮肽素,半胱氨酸蛋白酶抑制剂和胰蛋白酶样丝氨酸蛋白酶抑制剂,但不是广谱 MMP 抑制剂 marimastat,显著抑制观察到的归巢效应,并且这种抑制不是由于细胞毒性。此外,免疫沉淀 HTRA1,一种已知由分化为所有三种主要间充质谱系的细胞以及一般应激细胞分泌的胰蛋白酶样丝氨酸蛋白酶,并且已知降解包括胶原蛋白在内的许多基质蛋白,明显降低了归巢效应。数据表明,这种蛋白酶是观察到的骨髓基质细胞趋化性的主要贡献者。本研究表明,胶原蛋白片段可以介导骨髓基质细胞的迁移。结果还表明,至少在肌肉骨骼和脂肪组织中,基质重塑发生,通常与组织重塑密切相关,也应被视为潜在的干细胞募集事件。