Intravascular release of intact cellular fibronectin during oxidant-induced injury of the in vitro perfused rabbit lung.

Intravascular release of intact cellular fibronectin during oxidant-induced injury of the in vitro perfused rabbit lung.
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体外灌注兔肺氧化诱导损伤期间完整细胞纤连蛋白的血管内释放。

DOI:
10.1172/jci112752
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发表时间:
1986
期刊:
The Journal of clinical investigation
影响因子:
--
通讯作者:
Cochrane,CG
Cochrane,CG
中科院分区:
--
文献类型:
--
作者:
Peters,JH;Ginsberg,MH;Bohl,BP;Sklar,LA;Cochrane,CG

文献摘要

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纤连蛋白(Fn)是由体内炎症部位血管中的细胞产生的。因此,Fn释放到循环中可能是血管损伤的标志。在支持这一点,我们发现,氧化剂诱导的血管损伤的离体灌注兔肺引起循环Fn水平升高。Western印迹分析表明,Fn从损伤的血管释放是完整的,二聚体,并具有相同的Fn由成纤维细胞产生的电泳迁移率。与从兔血浆中分离的Fn不同,来源于肺灌注液或由成纤维细胞产生的Fn与抗体反应,所述抗体针对含有来自在成纤维细胞中转录而非肝细胞中转录的额外III型Fn结构域的序列的合成肽。蛋白酶引起的血管损伤也与血管内Fn的释放有关,但与裂解有关。氧化剂诱导的血管损伤导致组织来源的Fn释放,其可通过其大小和额外III型结构域的抗原决定簇含量与血浆Fn区分开来。图片
Fibronectin (Fn) is produced by cells in blood vessels at inflammatory sites in vivo. Fn release into the circulation thus may be a marker for vascular injury. In support of this, we found that oxidant-induced vascular injury of isolated perfused rabbit lungs caused elevated circulating Fn levels. Western blot analysis indicated that Fn released from the injured blood vessels was intact, dimeric, and possessed electrophoretic mobility identical with Fn produced by fibroblasts. Unlike Fn isolated from rabbit plasma, Fn derived from lung perfusate or produced by fibroblasts reacted with antibodies raised to a synthetic peptide containing sequences from the extra type III Fn domain that is transcribed in fibroblasts but not hepatocytes. Vascular injury by protease was also associated with intravascular release of Fn, but with cleavage. Oxidant-induced vascular injury causes release of tissue-derived Fn, which can be distinguished from plasma Fn by its size and content of antigenic determinants of the extra type III domain.Images