Effects of tumour necrosis factor and related cytokines on vascular endothelial cells.
Effects of tumour necrosis factor and related cytokines on vascular endothelial cells.
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肿瘤坏死因子及相关细胞因子对血管内皮细胞的影响。
DOI：
10.1002/9780470513521.ch12
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Pober,JS
中科院分区：
文献类型：
--
作者：
Pober,JS
肿瘤坏死因子（tumor necrosis factor，TNF）及其相关细胞因子可改变血管内皮细胞的表型，从而促进凝血、炎症和免疫。本研究采用重组人肿瘤坏死因子（TNF）、光敏素（LT）、白细胞介素1α（IL-1α）和白细胞介素1β（IL-1β），研究并比较了这些分子对培养的人内皮细胞（HEC）的作用。所有四种介质导致HEC单层从上皮样重组为成纤维细胞样形态。重组是缓慢的（数天），在细胞因子撤出后可逆，并通过免疫干扰素的共同添加而增强。与形态学变化一致，TNF和LT（而不是IL-1α或IL-1β）导致HLA-A、B mRNA和抗原表达显著增加。TNF和LT还诱导IL-1物质的mRNA水平和细胞表面表达缓慢增加。据报道，所有四种细胞因子均可增强淋巴细胞和炎性白细胞的HEC粘附;这些变化分别与细胞间粘附分子1（ICAM-1）表达的快速（小时）和持续增加以及内皮-白细胞粘附分子（通过抗体H4/18检测）的快速但短暂的新表达时间一致。TNF和LT诱导相互快速耐受，以重新诱导H4/18结合，但不抑制IL-1α和IL-1β的诱导;同样，IL-1α和IL-1β诱导相互快速耐受，但不抑制TNF或LT。我们使用H4/18的结合来探讨TNF的作用机制。发现促肿瘤的佛波酯（而不是增加细胞质钙浓度的药物）诱导结合，表明蛋白激酶C途径可能参与HEC对TNF的反应。用佛波醇酯预处理24小时的细胞不能被佛波醇酯再诱导表达H4/18结合，但仍保留对TNF的完全反应性。因此，TNF似乎也通过不依赖于蛋白激酶C活化的途径作用于HEC。总的来说，TNF和相关细胞因子的这些作用可以理解为内皮细胞活化的实例。
Tumour necrosis factor (TNF) and related cytokines have been found to alter the phenotype of vascular endothelial cells so as to promote coagulation, inflammation and immunity. We have used recombinant human TNF, lymphotoxin (LT), interleukin 1α (IL‐1α) and interleukin 1β (IL‐1β) to study and compare the effects of these molecules on cultured human endothelial cells (HEC). All four mediators cause HEC monolayers to reorganize from an epithelioid to a fibroblastoid morphology. Reorganization is slow (days), reversible upon cytokine withdrawal and enhanced by co‐addition of immune interferon. Coincident with morphological change, TNF and LT (but not IL‐1α or IL‐1β) cause a marked increase in HLA‐A, B mRNA and antigen expression. TNF and LT also induce a slow increase in the mRNA levels and cell‐surface expression of IL‐1 species. All four cytokines have been reported to enhance HEC adhesiveness for lymphocytes and inflammatory leucocytes; these changes temporally coincide with a rapid (hours) and sustained increase in expression of intercellular adhesion molecule 1 (ICAM‐1), and with a rapid but transientde novoexpression of an endothelial‐leucocyte adhesion molecule (detected by antibody H4/18), respectively. TNF and LT induce reciprocal tachyphylaxis for the reinduction of H4/18 binding but do not inhibit induction by IL‐1α and IL‐1β; similarly, IL‐1α and IL‐1β induce reciprocal tachyphylaxis but do not inhibit TNF or LT. We have used the binding of H4/18 to explore the mechanism of action of TNF. Tumour‐promoting phorbol esters, but not agents which increase cytoplasmic calcium concentrations, were found to induce binding, suggesting a possible involvement of the protein kinase C pathway in the response of HEC to TNF. Cells pretreated for 24 hours with phorbol esters cannot be reinduced to express H4/18 binding by phorbol esters yet retain full responsiveness to TNF. Thus TNF also appears to act on HEC through a pathway independent of protein kinase C activation. Collectively, these effects of TNF and related cytokines may be understood as examples of endothelial cell activation.
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DOI：
10.1073/pnas.80.15.4654
发表时间：
1983
影响因子：
11.1
作者：
Shaun J. Scahill;Rene Devos;Jose Van;Der;Heyden;W. Fiers
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DOI：
--
发表时间：
1987
期刊：
Virchows Archiv B Cell Pathology Including Molecular Pathology
影响因子：
--
作者：
C. Kuper;N. Bloksma;J. Bruyntjes;F. Hofhuis
通讯作者：
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肿瘤坏死因子诱导β2-干扰素：控制细胞增殖的稳态机制
影响因子：
64.5
作者：
M. Kohase;D. Henriksen‐Destefano;L. May;J. Vilček;P. Sehgal
通讯作者：
P. Sehgal
DOI：
10.1073/pnas.83.10.3460
发表时间：
1986-05-01
影响因子：
11.1
作者：
NAWROTH, PP;HANDLEY, DA;STERN, DM
通讯作者：
STERN, DM
DOI：
--
发表时间：
1986-08
期刊：
The American journal of pathology
影响因子：
--
作者：
P. Libby;J. Ordovás;K. Auger;A. Robbins;L. Birinyi;C. Dinarello
通讯作者：
P. Libby;J. Ordovás;K. Auger;A. Robbins;L. Birinyi;C. Dinarello