Hypothermia inhibits human E-selectin transcription.

Hypothermia inhibits human E-selectin transcription.
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低温抑制人类 E-选择素转录。

DOI:
10.1006/jsre.1996.0325
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发表时间:
1996
期刊:
The Journal of surgical research
影响因子:
--
通讯作者:
Verrier,ED
Verrier,ED
中科院分区:
--
文献类型:
--
作者:
Haddix,TL;Pohlman,TH;Noel,RF;Sato,TT;BoyleJr,EM;Verrier,ED

文献摘要

被引文献

相似文献

在内皮细胞活化过程中,E-选择素的形成和表达需要E-选择素基因的转录激活,其5′-侧翼区的多个转录因子和顺式作用元件的协同作用介导。据报道,体外低温(25°C)瞬时抑制E-选择素的转录激活和表面表达以及中性粒细胞对用脂多糖(LPS)、白介素-1(IL-1)或肿瘤坏死因子(TNF)处理的培养的人脐静脉内皮细胞(HUVEC)的粘附。将用LPS、IL-1或TNF处理的HUVEC复温至37°C恢复E-选择素转录物积累、E-选择素表面表达和中性粒细胞对HUVEC的粘附,其水平相当于连续维持在37°C的类似处理的HUVEC。尽管在25°C下没有可检测到的E-选择素转录,但在LPS、IL-1或TNF处理的HUVEC中仍然发生转录因子NF-κB的激活,表明信号转导没有被低温阻断。结论:低温可可逆性抑制E-选择素介导的中性粒细胞与活化内皮细胞的粘附。临床上低温的保护作用(例如,心肺旁路术)可以部分地通过瞬时抑制内皮细胞活化表型的表达来介导。
During endothelial cell activation, the formation and expression of E-selectin require transcriptional activation of the E-selectin gene, mediated by the coordinated action of several transcription factors andcis-acting elements in its 5′-flanking region. It is reported thatin vitrohypothermia (25°C) transiently inhibits transcriptional activation and surface expression of E-selectin as well as neutrophil adherence to cultured human umbilical vein endothelial cells (HUVECs) treated with lipopolysaccharide (LPS), interleukin-1 (IL-1), or tumor necrosis factor (TNF). Rewarming HUVECs treated with LPS, IL-1, or TNF to 37°C restores E-selectin transcript accumulation, E-selectin surface expression, and neutrophil adherence to HUVECs at levels equivalent to similarly treated HUVECs maintained at 37°C continuously. Despite the absence of detectable E-selectin transcription at 25°C, activation of the transcription factor NF-κB still occurred in HUVECs treated with LPS, IL-1, or TNF, indicating that signal transduction was not blocked by hypothermia. It is concluded that neutrophil adherence to activated endothelium mediated by E-selectin is reversibly inhibited by hypothermia. The protective effect of hypothermia clinically (e.g., cardiopulmonary bypass) may, in part, be mediated by transiently inhibiting the expression of an endothelial cell activation phenotype.