On the binding of tumor necrosis factor (TNF) to heparin and the release in vivo of the TNF-binding protein I by heparin.
On the binding of tumor necrosis factor (TNF) to heparin and the release in vivo of the TNF-binding protein I by heparin.
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关于肿瘤坏死因子 (TNF) 与肝素的结合以及肝素在体内释放 TNF 结合蛋白 I。
DOI：
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发表时间：
1991
影响因子：
15.9
通讯作者：
I. Olsson
中科院分区：
文献类型：
--
作者：
M. Lantz;H. Thysell;E. Nilsson;I. Olsson
肿瘤坏死因子是一种由激活的巨噬细胞释放的蛋白质，是宿主对感染和炎症反应的中心介质。肿瘤坏死因子结合蛋白I(TNF-BP-I)是p60跨膜型肿瘤坏死因子受体的可溶性片段，是肿瘤坏死因子的拮抗剂。肾功能不全患者血清肿瘤坏死因子-BP-I水平升高是肾小球滤过率下降的结果。在肾功能衰竭患者的血液透析过程中，血清中的肿瘤坏死因子-BP-I迅速而短暂地升高。这种增加被发现是由透析前给予肝素引起的，在健康个体中也观察到了类似的肝素剂量依赖性反应。发现在间歇注射肝素的情况下，肿瘤坏死因子-BP-I反复释放到循环中，这表明在储存池和循环池中都存在肿瘤坏死因子-BP-I。肝素介导的释放肿瘤坏死因子-BP-I的机制尚未解释；肿瘤坏死因子-BP与肝素没有亲和力。另一方面，发现肿瘤坏死因子与肝素有亲和力，也可以通过肿瘤坏死因子-BP-I将其与肝素解离。提示细胞外基质类肝素分子可以将肿瘤坏死因子保留在与靶细胞接近的物理位置，限制肿瘤坏死因子的作用，保护机体免受全身有害症状的侵害。
Tumor necrosis factor (TNF), a protein released by activated macrophages, is a central mediator of the host response to infection and inflammation. The TNF-binding protein I (TNF-BP-I) is a soluble fragment of the p60 transmembrane TNF receptor and an antagonist to TNF. The level of serum TNF-BP-I was found to be increased in patients with renal insufficiency as a result of a decrease in the glomerular filtration rate. During hemodialysis of patients with renal failure there was a rapid but transient increase in serum TNF-BP-I. This increase was found to be caused by heparin given before dialysis and a similar dose-dependent response to heparin was observed also in healthy individuals. The finding of a repeated release of TNF-BP-I into the circulation with intermittent injections of heparin indicates that TNF-BP-I is present both in a storage pool and in a circulating pool. The mechanism for the heparin-mediated release of TNF-BP-I was not explained; TNF-BP did not show affinity for heparin. On the other hand, TNF was found to have affinity for heparin and it could also be dissociated from heparin by TNF-BP-I. It is suggested that heparin-like molecules of the extracellular matrix can retain TNF in physical proximity with target cells and restrict the actions of TNF and protect against systemic harmful manifestations.
细胞表面硫酸肝素参与脂蛋白脂肪酶与培养的牛内皮细胞的结合。
DOI：
10.1172/jci110354
发表时间：
1981
期刊：
The Journal of clinical investigation
影响因子：
--
作者：
Shimada,K;Gill,PJ;Silbert,JE;Douglas,WH;Fanburg,BL
通讯作者：
Fanburg,BL
影响因子：
56.9
作者：
BEUTLER, B;MILSARK, IW;CERAMI, AC
通讯作者：
CERAMI, AC