S1P and eNOS regulation.
In the mammalian cardiovascular system, nitric oxide (NO), a small diffusible gaseous signal mediator, plays pivotal roles in the maintenance of vascular homeostasis. The endothelial isoform of nitric oxide synthase (eNOS) 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 analyzes the eNOS regulatory processes evoked by S1P. The implications of S1P activation of eNOS in cardiovascular (patho)physiology will be also discussed.
Igarashi
Junsuke
J
Department of Cardiovascular Physiology, Kagawa University Faculty of Medicine, 1750-1 Ikenobe, Miki-cho, Kita-gun, Kagawa, 761-0793 Japan. igarashi@med.kagawa-u.ac.jp
Michel
Thomas
T
D000818:Animals; D004789:Enzyme Activation; D006801:Humans; D008246:Lysophospholipids / Q000378:metabolism*; D018919:Neovascularization, Physiologic; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism*; D049349:Receptors, Lysosphingolipid / Q000378:metabolism; D015398:Signal Transduction; D013110:Sphingosine / Q000031:analogs & derivatives* / Q000378:metabolism
D008246:Lysophospholipids; D049349:Receptors, Lysosphingolipid; C060506:sphingosine 1-phosphate; D052250:Nitric Oxide Synthase Type III; D013110:Sphingosine