Sphingomyelinase causes endothelium-dependent vasorelaxation through endothelial nitric oxide production without cytosolic Ca2+ elevation
Sphingomyelinase causes endothelium-dependent vasorelaxation through endothelial nitric oxide production without cytosolic Ca2+ elevation
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DOI：
10.1016/j.febslet.2004.11.100
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发表时间：
2005-01-17
期刊：
影响因子：
3.5
通讯作者：
Kobayashi, S
中科院分区：
文献类型：
--
作者：
Mogami, K;Kishi, H;Kobayashi, S
中性鞘磷脂酶(N-sMase)可在不影响主动脉瓣内皮细胞内钙浓度([Ca~(2+)](I))的情况下，增加一氧化氮(NO)的生成，并诱导明显的内皮依赖性冠状动脉松弛，其作用可被一氧化氮合酶(NO)抑制剂N-omega-单甲基-L-精氨酸阻断。N-sMase诱导内皮型一氧化氮合酶(ENOS)从质膜小窝向胞内区移位，丝氨酸1179上eNOS磷酸化，内皮细胞神经酰胺水平升高。膜通透性神经酰胺(C-8-神经酰胺)模拟N-sMase的反应。我们认为N-sMase和神经酰胺参与了内皮细胞内钙非依赖性eNOS的激活和NO的产生，与内皮依赖性血管松弛有关。(C)2004年，由Elsevier B.V.代表欧洲生化学会联合会出版。
Neutral sphingomyelinase (N-SMase) elevated nitric oxide (NO) production without affecting intracellular Ca2+ concentration ([Ca2+](i)) in endothelial cells in situ on aortic valves, and induced prominent endothelium-dependent relaxation of coronary arteries, which was blocked by N-omega-monomethyl-L-arginine, a NO synthase (NOS) inhibitor. N-SMase induced translocation of endothelial NOS (eNOS) from plasma membrane caveolae to intracellular region, eNOS phosphorylation on serine 1179, and an increase of ceramide level in endothelial cells. Membrane-permeable ceramide (C-8-ceramide) mimicked the responses to N-SMase. We propose the involvement of N-SMase and ceramide in Ca2+-independent eNOS activation and NO production in endothelial cells in situ, linking to endothelium-dependent vasorelaxation. (C) 2004 Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies.