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用于胶原晶格收缩的细胞运动力与细胞收缩力:伤口收缩的体外模型

Cell locomotion forces versus cell contraction forces for collagen lattice contraction: an in vitro model of wound contraction.

作者信息

Ehrlich H P, Rajaratnam J B

机构信息

Shriner Burns Institute, Department of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston 02114.

出版信息

Tissue Cell. 1990;22(4):407-17. doi: 10.1016/0040-8166(90)90070-p.

DOI:10.1016/0040-8166(90)90070-p
PMID:2260082
Abstract

Cultured human dermal fibroblasts suspended in a rapidly polymerizing collagen matrix produce a fibroblast-populated collagen lattice. With time, this lattice will undergo a reduction in size referred to as lattice contraction. During this process, two distinct cell populations develop. At the periphery of the lattice, highly oriented sheets of cells, morphologically identifiable as myofibroblasts, show cell-to-cell contacts and thick, actin-rich staining cytoplasmic stress fibers. It is proposed that these cells undergoing cell contraction produce a multicellular contractile unit which reorients the collagen fibrils associated with them. The cells in the central region, referred to as fibroblasts, are randomly oriented, with few cell-to-cell contacts and faintly staining actin cytoplasmic filaments. In contrast it is proposed that cells working as single units use cell locomotion forces to reorient the collagen fibrils associated with them. Using this model, we sought to determine which of these two mechanisms, cell contraction or cell locomotion, is responsible for the force that contracts collagen lattices. Our experiments showed that fibroblasts produce this contractile force, and that the mechanism for lattice contraction appears to be related to cell locomotion. This is in contrast to a myofibroblast; where the mechanism for contraction is based upon cell contractions. Fibroblasts attempting to move within the collagen matrix reorganize the surrounding collagen fibrils; when these collagen fibrils can be organized no further and cell-to-cell contacts develop, which occurs at the periphery of the lattice first, these cells can no longer participate in the dynamic aspects of lattice contraction.

摘要

悬浮在快速聚合胶原基质中的培养人真皮成纤维细胞可形成成纤维细胞填充的胶原晶格。随着时间的推移,这种晶格会经历尺寸减小,即晶格收缩。在此过程中,会形成两个不同的细胞群体。在晶格的周边,高度定向的细胞片层,形态上可识别为肌成纤维细胞,显示细胞间接触以及粗大的、富含肌动蛋白染色的细胞质应力纤维。有人提出,这些经历细胞收缩的细胞产生一个多细胞收缩单元,该单元可重新定向与其相关的胶原纤维。中心区域的细胞,称为成纤维细胞,随机定向,细胞间接触少,肌动蛋白细胞质细丝染色浅。相反,有人提出作为单个单元起作用的细胞利用细胞运动力来重新定向与其相关的胶原纤维。利用这个模型,我们试图确定这两种机制,即细胞收缩还是细胞运动,是导致胶原晶格收缩力的原因。我们的实验表明,成纤维细胞产生这种收缩力,并且晶格收缩机制似乎与细胞运动有关。这与肌成纤维细胞不同,肌成纤维细胞的收缩机制基于细胞收缩。试图在胶原基质内移动的成纤维细胞会重组周围的胶原纤维;当这些胶原纤维无法进一步组织且细胞间接触形成时,这种情况首先发生在晶格的周边,这些细胞就不再参与晶格收缩的动态过程。

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