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培养的掌腱膜挛缩症和正常掌部成纤维细胞产生收缩力的情况。

Generation of contractile force by cultured Dupuytren's disease and normal palmar fibroblasts.

作者信息

Rayan G M, Tomasek J J

机构信息

Orthopedic Surgery Department, University of Oklahoma Health Sciences Center, Oklahoma City 73190, USA.

出版信息

Tissue Cell. 1994 Oct;26(5):747-56. doi: 10.1016/0040-8166(94)90057-4.

Abstract

Contractile fibroblasts are believed to be responsible for palmar fascia contracture in Dupuytren's Disease. An in vitro collagen lattice model was used to examine the contractile properties of Dupuytren's fibroblasts from 10 patients undergoing partial fasciectomy, and palmar fascia fibroblasts from 6 patients undergoing carpel tunnel release. Dupuytren's and palmar fascia fibroblasts cultured within a stabilized collagen lattice acquired morphological characteristics similar to those of 'myofibroblasts' in Dupuytren's diseased fascia. Both types of fibroblasts generated contractile forces that resulted in rapid collagen lattice contraction after release of the lattice from points of stabilization. Generation of contractile force by the fibroblasts was inhibited by disruption of the actin cytoskeleton, lack of cells, or serum removal. Afferent neuropeptides (substance P, galanin and neurokinin A) did not promote lattice contraction. These results demonstrate that normal palmar fascia fibroblasts can modulate into Dupuytren's-like fibroblasts and that cultured fibroblasts, from either Dupuytren's diseased or normal palmar fascia, can generate contractile forces that are transmitted to extracellular matrix. In addition, fibroblast contraction is an actin based process which requires specific factor(s) present in serum. It is suggested that in Dupuytren's disease extracellular cues trigger the modulation of fibroblasts to Dupuytren's fibroblasts and the promotion of contractile forces responsible for palmar fascia contrature.

摘要

收缩性成纤维细胞被认为是导致掌腱膜挛缩症(Dupuytren病)的原因。采用体外胶原晶格模型,检测了10例接受部分筋膜切除术患者的Dupuytren成纤维细胞以及6例接受腕管松解术患者的掌腱膜成纤维细胞的收缩特性。在稳定的胶原晶格中培养的Dupuytren成纤维细胞和掌腱膜成纤维细胞获得了与Dupuytren病筋膜中“肌成纤维细胞”相似的形态特征。两种类型的成纤维细胞均产生收缩力,导致胶原晶格从固定点释放后迅速收缩。肌动蛋白细胞骨架的破坏、细胞缺失或血清去除均抑制了成纤维细胞收缩力的产生。传入神经肽(P物质、甘丙肽和神经激肽A)并未促进晶格收缩。这些结果表明,正常掌腱膜成纤维细胞可转变为类似Dupuytren病的成纤维细胞,并且来自Dupuytren病或正常掌腱膜的培养成纤维细胞均可产生传递至细胞外基质的收缩力。此外,成纤维细胞收缩是一个基于肌动蛋白的过程,需要血清中存在特定因子。提示在Dupuytren病中,细胞外信号触发成纤维细胞向Dupuytren成纤维细胞的转变以及导致掌腱膜挛缩的收缩力的增强。

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