Fibrin degradation by rat pulmonary alveolar epithelial cells.
Fibrin degradation by rat pulmonary alveolar epithelial cells.
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大鼠肺泡上皮细胞的纤维蛋白降解。
DOI：
10.1152/ajplung.1992.262.4.l482
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Sitrin,RG
中科院分区：
文献类型：
--
作者：
Simon,RH;Gross,TJ;Edwards,JA;Sitrin,RG
在急性和慢性炎症性肺部疾病中，肺泡内纤维蛋白的持续存在表明，作为疾病过程的一部分，肺泡腔的正常纤溶环境已经改变。我们最近发现肺泡上皮细胞可能通过表达尿激酶型纤溶酶原激活物(UPA)和纤溶酶原激活物抑制物-1来控制纤溶。在本研究中，大鼠肺泡上皮细胞单层被用作肺泡表面的模型，并被发现通过纤溶酶原和uPA依赖的过程来溶解血浆来源的纤维蛋白基质。纤溶不是通过液体相上皮产品实现的，但需要上皮细胞的存在，最好是与血栓表面密切接触。内皮细胞介导的纤溶活性可被内毒素增强99%，而被地塞米松抑制66%。随着细胞在培养的第1天至第4天的老化，纤溶活性也增加了84%，在此期间，细胞失去了许多II型细胞的特征，并呈现I型细胞样表型。我们得出结论，肺泡上皮细胞通过要求上皮细胞和凝块表面紧密接触的机制，积极参与纤维蛋白的清除。这些机制的改变可能是肺炎症期间肺泡内纤维蛋白持续存在的部分原因。
The persistence of intra-alveolar fibrin during acute and chronic inflammatory lung diseases indicates that the normally profibrinolytic environment of the alveolar space has been altered as part of the disease process. We have recently shown that alveolar epithelial cells may control fibrinolysis by expressing both urokinase-type plasminogen activator (uPA) and plasminogen activator inhibitor-1. In this study, monolayers of rat alveolar epithelial cells were used as a model of the alveolar surface and were found to lyse plasma-derived fibrin matrices by a process that was plasminogen and uPA dependent. Fibrinolysis was not achieved by fluid-phase epithelial products but required the presence of epithelial cells, optimally in close contact with the clot surface. Epithelial cell-mediated fibrinolytic activity was augmented 99% by endotoxin and suppressed 66% by dexamethasone. Fibrinolysis also increased 84% as cells aged in culture from day 1 to day 4, during which time the cells lose many type II cell characteristics and assume a type I cell-like phenotype. We conclude that alveolar epithelial cells actively participate in fibrin clearance through mechanisms that require close proximity between epithelial cell and clot surfaces. Alterations in these mechanisms may be partly responsible for the persistence of intraalveolar fibrin during lung inflammation.