Theory of intercellular communication in the development of endothelial dysfunction.

Activation of intracellular signaling and blebbing of the plasma membrane lead to rafting and clustering of membrane receptors. Lymphocyte with high receptor density at the cell pole interacts with endothelial cells, which leads to their hyperactivation. In this case, lymphocyte getting a response from the endothelial cell can release membrane particles, which interact with endothelial receptors and penetrate through gaps between endothelial cells forming aseptic inflammation and causing atherogenesis. Endotheliocytes also contribute to generation of active membrane microparticles. Hyperactivation of endothelial cells and constant stimulation by the lymphocytes and microparticles trigger programmed cell death resulting in exfoliation of the endothelial cell. The endothelial defect is replaced by endothelial cells of the vascular wall (in case of mild endothelial dysfunction) or by progenitor endothelial cells (in case of severe dysfunction).