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REVIEW: Lipid Second Messengers and Cell Signaling in Vascular Wall

N. V. Prokazova*, N. N. Samovilova, N. K. Golovanova, E. V. Gracheva, A. A. Korotaeva, and E. R. Andreeva

Institute of Experimental Cardiology, Russian Cardiology Research Center, 3-ya Cherepkovskaya ul. 15a, 121552 Moscow, Russia; fax: (495) 149-0559; E-mail: prokazova@cardio.ru

* To whom correspondence should be addressed.

Received January 24, 2007; Revision received April 26, 2007
Agonists of cellular receptors, such as receptor tyrosine kinases, G protein-coupled receptors, cytokine receptors, etc., activate phospholipases (Cgamma, Cbeta, A2, D), sphingomyelinase, and phosphatidylinositol-3-kinase. This produces active lipid metabolites, some of which are second messengers: inositol trisphosphate, diacylglycerides, ceramide, and phosphatidylinositol 3,4,5-trisphosphate. These universal mechanisms are involved in signal transduction to maintain blood vessel functions: regulation of vasodilation and vasoconstriction, mechanical stress resistance, and anticoagulant properties of the vessel lumen surface. Different signaling pathways realized through lipid second messengers interact to one another and modulate intracellular events. In early stages of atherogenesis, namely, accumulation of low density lipoproteins in the vascular wall, cascades of pro-atherogenic signal transduction are triggered through lipid second messengers. This leads to atherosclerosis, the general immuno-inflammatory disease of the vascular system.
KEY WORDS: phospholipases, phospholipids, inositol 1,4,5-trisphosphate, phosphatidylinositol 3,4,5-trisphosphate, diacylglycerides, ceramide, endothelial and smooth muscle vascular cells

DOI: 10.1134/S0006297907080019