The effects of markedly raised intracellular sphingosine kinase-1 activity in endothelial cells.
The effects of markedly raised intracellular sphingosine kinase-1 activity in endothelial cells.
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DOI：
10.2478/s11658-009-0008-2
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发表时间：
2009
影响因子：
8.3
通讯作者：
Gamble JR
中科院分区：
文献类型：
--
作者：
Limaye V;Vadas MA;Pitson SM;Gamble JR
鞘氨醇激酶-1 （SK1）促进鞘氨醇-1-磷酸（S1P）的形成，这是内皮细胞（EC）的重要存活因子。已知EC中细胞内SK1活性的适度增加可赋予细胞生存优势。在这里，我们研究了EC中细胞内SK1更急剧增加的影响。我们发现这些细胞在应激条件下表现出细胞存活率降低、caspase-3活性增强、细胞周期抑制和细胞-细胞连接破坏。我们提出，酶磷酸化状态的改变可能解释了SK1适度和高水平强制表达对表型的不同影响。我们的研究结果表明，SK1活性在EC中受到控制，而这种控制可能在涉及血管退化的情况下失去。
The enzyme sphingosine kinase-1 (SK1) promotes the formation of sphingosine-1-phosphate (S1P), which is an important survival factor for endothelial cells (EC). Modest increases in intracellular SK1 activity in the EC are known to confer a survival advantage upon the cells. Here, we investigated the effects of more dramatic increases in intracellular SK1 in the EC. We found that these cells show reduced cell survival under conditions of stress, enhanced caspase-3 activity, cell cycle inhibition, and cell-cell junction disruption. We propose that alterations in the phosphorylation state of the enzyme may explain the differential effects on the phenotype with modest versus high levels of enforced expression of SK1. Our results suggest that SK1 activity is subject to control in the EC, and that this control may be lost in conditions involving vascular regression.
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影响因子：
4.8
作者：
Kwon, YG;Min, JK;Kim, YM
通讯作者：
Kim, YM
影响因子：
56.9
作者：
Lee, MJ;Van Brocklyn, JR;Hla, T
通讯作者：
Hla, T
影响因子：
9.2
作者：
Xia, P;Gamble, JR;Vadas, MA
通讯作者：
Vadas, MA
DOI：
10.1073/pnas.95.24.14196
发表时间：
1998-11-24
影响因子：
11.1
作者：
Xia, P;Gamble, JR;Vadas, MA
通讯作者：
Vadas, MA
影响因子：
4.8
作者：
Wang, F;Van Brocklyn, JR;Spiegel, S
通讯作者：
Spiegel, S