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炎症中的纤溶酶原激活系统。

The plasminogen activation system in inflammation.

作者信息

Del Rosso Mario, Fibbi Gabriella, Pucci Marco, Margheri Francesca, Serrati Simona

机构信息

Department of Experimental Pathology and Oncology, University of Florence, Viale G.B. Morgagni, 50, 50134, Florence, Italy.

出版信息

Front Biosci. 2008 May 1;13:4667-86. doi: 10.2741/3032.

DOI:10.2741/3032
PMID:18508538
Abstract

Inflammation is an adaptive response to damage of vascularized tissues, which develops according to a stereotyped sequence governed by the local production of the so-called "chemical mediators of inflammation". Here we review the evidences indicating a role of the plasminogen activation system in the regulation of all the phases of the inflammation process. Plasminogen activation controls the formation of complement anaphylotoxins (responsible for vasodilatation, increase of venular permeability and leukocyte chemotaxis) and of bradykinin (which accounts for vasodilatation, increase of venular permeability and pain) by regulating the plasma contact system. The urokinase plasminogen activator and its cellular receptor, expressed on the surface of human leukocytes, provide a functional unit that, by regulating interaction of leukocytes with extracellular matrix, as well as its degradation, is critical for the migration of leukocytes and for their movement in the damaged tissues. By preventing excess fibrin accumulation in inflamed tissues, the plasminogen activation system also governs the proper evolution of the inflammatory exudates and prevents the possibility of a shift from acute to chronic inflammation.

摘要

炎症是血管化组织损伤后的一种适应性反应,它按照由所谓的“炎症化学介质”局部产生所控制的固定顺序发展。在此,我们综述了表明纤溶酶原激活系统在炎症过程所有阶段调节中发挥作用的证据。纤溶酶原激活通过调节血浆接触系统来控制补体过敏毒素(负责血管舒张、小静脉通透性增加和白细胞趋化性)和缓激肽(导致血管舒张、小静脉通透性增加和疼痛)的形成。尿激酶型纤溶酶原激活剂及其在人白细胞表面表达的细胞受体构成一个功能单元,该单元通过调节白细胞与细胞外基质的相互作用及其降解,对白细胞的迁移及其在受损组织中的移动至关重要。通过防止炎症组织中纤维蛋白过度积聚,纤溶酶原激活系统还控制着炎性渗出物的正常演变,并防止从急性炎症转变为慢性炎症的可能性。

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