Shear stress increases the amount of S‐nitrosylated molecules in endothelial cells: important role for signal transduction

FEBS Letters

Haendeler, Judith¹  Dimmeler, Stefanie¹  Hoffmann, Jörg¹ 

[1] Molecular Cardiology, Department of Internal Medicine IV, University of Frankfurt, Theodor-Stern-Kai 7, Frankfurt, Germany

关键词: Caspase;    Endothelial cell;    GTPase p21ras;    S-nitrosylation;    Shear stress;    Thioredoxin;    HUVEC;    human umbilical vein endothelial cells;    HUAEC;    human arterial endothelial cells;    NOS;    nitric oxide synthase;    NO;    nitric oxide;    DAN;    2;    3-diamino-naphthalene;    L-NMMA;    NG-monomethyl-L-arginine;   

DOI  :  10.1016/S0014-5793(03)00917-7

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Laminar flow (shear stress) is an important stimulus for nitric oxide (NO) synthesis in endothelial cells. NO can react with free SH-groups of different proteins leading to S-nitrosylation. Since S-nitrosylation of proteins is an important regulator of protein functions, we investigated the effect of endogenously synthesized NO. Exposure to shear stress significantly increased the overall S-nitrosylation of proteins in endothelial cells. Interestingly, shear stress increased S-nitrosylation of specific target proteins, i.e. the catalytic p17 subunit of caspase-3, the GTPase p21ras and the oxidoreductase thioredoxin. S-nitrosylation resulted in an inhibition of caspase-3 and in an augmented activity of p21ras and thioredoxin. These data suggest that long term exposure to shear stress exerts its different atheroprotective effects at least in part via increased S-nitrosylation of specific signaling proteins.

【 授权许可】

Unknown