Noninflammatory expression of E-selectin is regulated by cell growth
Noninflammatory expression of E-selectin is regulated by cell growth
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DOI：
10.1182/blood.v93.11.3785.411a44_3785_3791
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发表时间：
1999-06-01
期刊：
影响因子：
20.3
通讯作者：
Bischoff, J
中科院分区：
文献类型：
--
作者：
Luo, JY;Paranya, G;Bischoff, J
E-选择素是一种内皮特异性粘附分子，其在白细胞粘附中的作用最为人所知，在静止内皮细胞中未检测到，但由炎症刺激诱导。然而，E-选择素也在体内和体外非炎症条件下增殖的内皮细胞中表达，表明E-选择素也受生长信号调节。为了研究E-选择素在脂多糖刺激与非刺激的增殖细胞中的表达，我们分析了两种条件下E-选择素阳性的人微血管内皮细胞在细胞周期G（0）/G（1）、S和G（2）/M期的分布。脂多糖处理导致G（0）/G（1）、S和G（2）/M细胞中E-选择素表达均匀增加。相反，未受刺激的增殖细胞中E-选择素水平与G（2）/M细胞百分比呈线性相关。E-选择素在增殖的内皮细胞中没有减少通过添加可溶性肿瘤坏死因子-α-受体或可溶性白细胞介素-1-受体，表明其表达不是由于内源性产生的细胞因子。此外，E-选择素在用碱性成纤维细胞生长因子（一种众所周知的内皮细胞有丝分裂原）刺激的细胞中增加。增殖内皮细胞中的E-选择素是功能性的，如前髓细胞白血病细胞系HL-60与亚融合的人微血管内皮细胞的E-选择素依赖性粘附所示。总之，这些研究表明，E-选择素可以通过与内皮细胞增殖状态相关的非炎症途径进行调节。(C)1999年，美国血液学会。
E-selectin, an endothelial-specific adhesion molecule best known for its role in leukocyte adhesion, is not detected in quiescent endothelial cells, but is induced by inflammatory stimuli. However, E-selectin is also expressed in proliferating endothelial cells under noninflammatory conditions in vivo and in vitro, suggesting that E-selectin is also regulated by growth signals. To investigate E-selectin expression in lipopolysaccharide-stimulated versus nonstimulated proliferating cells, we analyzed the distribution of E-selectin-positive human microvascular endothelial cells in G(0)/G(1), S, and G(2)/M phases of the cell cycle under both conditions. Lipopolysaccharide treatment resulted in uniformly increased E-selectin expression in cells in G(0)/G(1), S, and G(2)/M. In contrast, levels of E-selectin in nonstimulated proliferating cells showed a linear correlation with the percentage of cells in G(2)/M. E-selectin in proliferating endothelial cells was not reduced by addition of soluble tumor necrosis factor-alpha-receptor or soluble interleukin-1-receptor indicating that its expression was not due to endogenous production of either cytokine. In addition, E-selectin was increased in cells stimulated with basic fibroblast growth factor, a well-known mitogen for endothelial cells. E-selectin in proliferating endothelial cells is functional, as shown by E-selectin-dependent adhesion of the promyelocytic leukemia cell line HL-60 to subconfluent human microvascular endothelial cells. In summary, these studies indicate that E-selectin can be regulated by a noninflammatory pathway that is related to the proliferative state of the endothelium. (C) 1999 by The American Society of Hematology.