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

Mechanisms by which fibrin and fibronectin appear in healing wounds: implications for Peyronie's disease.
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纤维蛋白和纤连蛋白在伤口愈合中出现的机制:对佩罗尼氏病的影响。

DOI:
10.1097/00005392-199701000-00103
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发表时间:
1997
期刊:
The Journal of urology
影响因子:
--
通讯作者:
VandeWater,L
VandeWater,L
中科院分区:
--
文献类型:
--
作者:
VandeWater,L

文献摘要

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目的在大多数情况下,存在于组织修复部位的细胞外基质经历了从含纤维蛋白的基质到富含胶原的瘢痕的有序转变。然而,在某些情况下,如佩罗尼病,纤维蛋白持续存在。许多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起重要作用。因此,纤维蛋白基质的存在可能在正常或致病性伤口愈合过程中具有重要意义,如佩罗尼氏病中所发生的。本研究采用原位杂交、免疫定位和标记示踪技术等方法,研究了创伤组织中纤维蛋白临时基质的形成机制。结果通过这些方法,我们发现创伤组织中纤维蛋白临时基质的形成主要有两种机制:血浆纤维连接蛋白和纤维蛋白原的渗漏,和纤连蛋白的变体的伤口cells. ConclusionsDeveloping了解的机制,调节这些基质蛋白的外观可能提供新的途径,如佩罗尼氏病的临时基质沉积的时间模式异常的条件下治疗。
PurposeThe 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 MethodsMethodologies, such as in situ hybridization, immunolocalization and labeled tracer techniques, were used in our study.ResultsWe 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.ConclusionsDeveloping 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.