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掌腱膜挛缩症的胶原变化

The collagen changes of Dupuytren's contracture.

作者信息

Murrell G A, Francis M J, Bromley L

机构信息

Nuffield Department of Orthopaedic Surgery, University of Oxford.

出版信息

J Hand Surg Br. 1991 Aug;16(3):263-6. doi: 10.1016/0266-7681(91)90050-x.

Abstract

In Dupuytren's contracture there is an increase in the ratio of type III to type I collagen. The objective of this study was to determine if fibroblasts from patients with Dupuytren's contracture have an intrinsic aberration in collagen production or whether local factors govern the collagen changes in Dupuytren's contracture. Using a new collagen micro-method, we found that fibroblasts cultured from palmar fascia affected by Dupuytren's contracture produced similar collagen to fibroblasts derived from the palmar fascia of age- and sex-matched patients with carpal tunnel syndrome. Furthermore, the collagen changes of Dupuytren's contracture could be reproduced in all cell lines by increasing fibroblast density. At high fibroblast density, type I collagen production was inhibited: a finding that could account for the increased types III/I collagen ratio in Dupuytren's contracture. These results suggest that a genetic defect in collagen production is unlikely and that the important phenomenon is an increase in fibroblast density.

摘要

在掌腱膜挛缩症中,III型胶原蛋白与I型胶原蛋白的比例增加。本研究的目的是确定掌腱膜挛缩症患者的成纤维细胞在胶原蛋白产生方面是否存在内在异常,或者局部因素是否控制着掌腱膜挛缩症中的胶原蛋白变化。使用一种新的胶原蛋白微量方法,我们发现从受掌腱膜挛缩症影响的掌腱膜培养的成纤维细胞产生的胶原蛋白与来自年龄和性别匹配的腕管综合征患者掌腱膜的成纤维细胞相似。此外,通过增加成纤维细胞密度,可以在所有细胞系中重现掌腱膜挛缩症的胶原蛋白变化。在高成纤维细胞密度下,I型胶原蛋白的产生受到抑制:这一发现可以解释掌腱膜挛缩症中III/I型胶原蛋白比例增加的原因。这些结果表明,胶原蛋白产生的遗传缺陷不太可能,重要的现象是成纤维细胞密度增加。

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