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尿激酶型纤溶酶原激活剂在迁移的毛细血管内皮细胞中被诱导产生。

Urokinase-type plasminogen activator is induced in migrating capillary endothelial cells.

作者信息

Pepper M S, Vassalli J D, Montesano R, Orci L

机构信息

Institute of Histology and Embryology, University of Geneva Medical Center, Switzerland.

出版信息

J Cell Biol. 1987 Dec;105(6 Pt 1):2535-41. doi: 10.1083/jcb.105.6.2535.

DOI:10.1083/jcb.105.6.2535
PMID:3121633
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2114714/
Abstract

Cellular migration is an essential component of invasive biological processes, many of which have been correlated with an increase in plasminogen activator production. Endothelial cell migration occurs in vivo during repair of vascular lesions and angiogenesis, and can be induced in vitro by wounding a confluent monolayer of cells. By combining the wounded monolayer model with a substrate overlay technique, we show that cells migrating from the edges of an experimental wound display an increase in urokinase-type plasminogen activator (uPA) activity, and that this activity reverts to background levels upon cessation of movement, when the wound has closed. Our results demonstrate a direct temporal relationship between endothelial cell migration and uPA activity, and suggest that induction of uPA activity is a component of the migratory process.

摘要

细胞迁移是侵袭性生物学过程的一个重要组成部分,其中许多过程都与纤溶酶原激活物产量的增加有关。内皮细胞迁移在体内血管损伤修复和血管生成过程中发生,并且在体外可以通过划伤汇合的单层细胞来诱导。通过将划伤的单层模型与底物覆盖技术相结合,我们发现从实验伤口边缘迁移的细胞显示出尿激酶型纤溶酶原激活物(uPA)活性增加,并且当伤口愈合、细胞停止移动时,这种活性恢复到背景水平。我们的结果证明了内皮细胞迁移与uPA活性之间存在直接的时间关系,并表明uPA活性的诱导是迁移过程的一个组成部分。

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A MOLECULAR MECHANISM OF MITOMYCIN ACTION: LINKING OF COMPLEMENTARY DNA STRANDS.丝裂霉素作用的分子机制:互补DNA链的连接
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