Chapter 10 Vascular endothelium and the blood–brain barrier

Abstract

This chapter describes the relation between vascular endothelium and the blood–brain barrier with regard to ischemia. The vascular endothelium helps in long-term control of vascular pathophysiology and disease progression. Apart from providing the lining of the vessel, endothelial cells perform and control many functions such as cell migration, remodeling, proliferation, apoptosis, the production, secretion, and metabolism of proteins and small molecules, and the regulation of the contractility of vascular smooth muscle cells. The endothelial response to ischemia differs from other endothelium, as cerebral endothelial cells are the important blood–brain interface in the modular system, termed as the blood–brain barrier. The cerebral endothelial cells of brain capillaries are unique in the vertebrae by virtue of their intimate cell–cell contacts, the tight junction, allowing only a little paracellular diffusion and only highly selective transendothelial transport. The brain capillary network and thus, the biology of the blood–brain barrier is critically dependent on the paracrine interaction between cerebral endothelial cells and pericytes, microglia, and astrocyte foot processes. As a prominent and characteristic feature of the blood–brain barrier, the tight junctions of cerebral endothelial cells differ considerably from other endo- and epithelial cells in other organ systems. The most important pathophysiological consequence of cerebral ischemia to the blood–brain barrier is the loss of barrier function, often termed blood–brain barrier disruption, opening, or leakage. Blood–brain barrier leakage, however, comprises not only loss of tight junction function but also degradation of basal lamina matrix proteins and alterations of the glia limitans formed by astrocyte end feet.