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

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Abstract
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.