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纤维蛋白和纤连蛋白在愈合伤口中出现的机制:对佩罗尼氏病的影响。

Mechanisms by which fibrin and fibronectin appear in healing wounds: implications for Peyronie's disease.

作者信息

Van de Water L

机构信息

Department of Pathology, Beth Israel Hospital, Boston, Massachusetts, USA.

出版信息

J Urol. 1997 Jan;157(1):306-10. doi: 10.1097/00005392-199701000-00103.

DOI:10.1097/00005392-199701000-00103
PMID:8976286
Abstract

PURPOSE

The extracellular matrix that is present at sites of tissue repair in most instances undergoes an orderly transition from a fibrin containing matrix to collagen-rich scar. However, in some conditions, such as Peyronie's disease, fibrin persists. Evidence from a number of experimental systems indicates that extracellular matrix proteins and their receptors serve an important function in regulating cell behaviors. Thus, the presence of the fibrin matrix is likely to have important implications in the course of either normal or pathogenic wound healing as occurs in Peyronie's disease. Potential mechanisms by which the fibrin rich provisional matrix appears in healing wounds are presented.

MATERIALS AND METHODS

Methodologies, such as in situ hybridization, immunolocalization and labeled tracer techniques, were used in our study.

RESULTS

We found by these approaches that the 2 general mechanisms that contribute to the generation of the wound extracellular matrix are leakage of plasma proteins, such as plasma fibronectin and fibrinogen, and the synthesis of variants of fibronectin by wound cells.

CONCLUSIONS

Developing an understanding of the mechanisms that regulate the appearance of these matrix proteins may provide new avenues for therapy in conditions such as Peyronie's disease in which the temporal pattern of the provisional matrix deposition is abnormal.

摘要

目的

在大多数情况下,组织修复部位存在的细胞外基质会经历从含纤维蛋白的基质到富含胶原蛋白的瘢痕的有序转变。然而,在某些情况下,如佩罗尼氏病,纤维蛋白会持续存在。来自多个实验系统的证据表明,细胞外基质蛋白及其受体在调节细胞行为中发挥着重要作用。因此,纤维蛋白基质的存在可能对正常或病理性伤口愈合过程具有重要影响,如佩罗尼氏病中发生的情况。本文介绍了富含纤维蛋白的临时基质出现在愈合伤口中的潜在机制。

材料与方法

我们的研究使用了原位杂交、免疫定位和标记示踪技术等方法。

结果

通过这些方法,我们发现导致伤口细胞外基质产生的两种一般机制是血浆蛋白(如血浆纤连蛋白和纤维蛋白原)的渗漏以及伤口细胞合成纤连蛋白变体。

结论

深入了解调节这些基质蛋白出现的机制可能为佩罗尼氏病等疾病提供新的治疗途径,在这些疾病中临时基质沉积的时间模式是异常的。

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