Functional role of TRPC channels in the regulation of endothelial permeability

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Abstract
The endothelial cells (ECs) form a semipermeable barrier between the blood and the tissue. An important function of the endothelium is to maintain the integrity of the barrier function of the vessel wall. Ca2+ signaling in ECs plays a key role in maintaining the barrier integrity. Transient receptor potential canonical (TRPC) channels are mammalian homologs of Drosophila TRP Ca2+-permeable channels expressed in EC. TRPC channels are thought to function as a Ca2+ entry channel operated by store-depletion as well as receptor-activated channels in a variety of cell types, including ECs. Inflammatory mediators such as thrombin, histamine, bradykinin, and others increase endothelial permeability by actin polymerization-dependent EC rounding and formation of inter-endothelial gaps, a process critically dependent on the increase in EC cytosolic [Ca2+] ([Ca2+]i). Increase in endothelial permeability depends on both intracellular Ca2+ release and extracellular Ca2+ entry through TRPC channels. This review summarizes recent findings on the role of TRPC channels in the mechanism of Ca2+ entry in ECs, and, in particular, the role of TRPC channels in regulating endothelial barrier function.