S1P and eNOS regulation

被引：43

作者：

Igarashi, Junsuke ^{[1
]}

Michel, Thomas ^{[2
,3
]}

机构：

[1] Kagawa Univ, Fac Med, Dept Cardiovasc Physiol, Miki, Kagawa 7610793, Japan

[2] Brigham & Womens Hosp, Div Cardiovasc, Dept Med, Boston, MA 02115 USA

[3] Harvard Univ, Sch Med, Boston, MA 02115 USA

来源：

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS | 2008年 / 1781卷 / 09期

关键词：

eNOS; caveolae; G-protein coupled receptors; vascular signaling; sphingosine; 1-phosphate; VEGF;

D O I：

10.1016/j.bbalip.2008.06.008

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

In the mammalian cardiovascular system, nitric oxide (NO), a small diffusible gaseous signal inediator, plays pivotal roles in the maintenance of vascular hormeostasis. The endothelial isoform of nitric oxide synthase (eNDS) is activated by diverse agonist-modulated cell surface receptors, and eNOS-derived NO is a key determinant of blood pressure, platelet activation, angiogenesis and other fundamental responses in the vascular wall. Sphingosine 1-phosphate (S1P) has recently been identified as an important activator of eNOS. This review summarizes the roles of sphingosine 1-phosphate and S1P receptors in eNOS activation. and eNOS analyzes the eNOS regulatory processes evoked by S1P. The implications of S1P activation of eNOS in Caveolae cardiovascular (patho)physiology will be also discussed. (c) 2008 Elsevier B.V. All rights reserved.

引用

页码：489 / 495

页数：7

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