Intercellular adhesion molecule 1 activation induces tyrosine phosphorylation of the cytoskeleton-associated protein cortactin in brain microvessel endothelial cells.

Inflammatory diseases of the central nervous system, such as multiple sclerosis or experimental autoimmune encephalomyelitis, are characterized by adhesion of lymphocytes on cerebral microvascular endothelium, followed by transendothelial migration into the brain parenchyma. T lymphocyte adhesion to vascular endothelial cells is mediated by several types of adhesion molecules, including the integrin leukocyte function-associated molecule 1 and its endothelial counter receptor intercellular adhesion molecule 1 (ICAM-1), of the immunoglobulin superfamily. In order to understand the molecular mechanisms that support lymphocyte extravasation, we intended to investigate a putative role of ICAM-1 in signal transduction in brain microvessel endothelial cells.

Regulation of gamma-glutamyl transpeptidase and alkaline phosphatase activities in immortalized rat brain microvessel endothelial cells.

Rat brain microvessel endothelial cells were immortalized by transfection with a plasmid containing the E1A adenovirus gene. One clone, called RBE4, was further characterized. These cells display a nontransformed phenotype and express typical endothelial markers, Factor VIII-related antigen and Bandeiraea simplicifolia binding sites.

Nitric oxide and endothelin secretion by brain microvessel endothelial cells: regulation by cyclic nucleotides.

Endothelin (ET)-1 was originally characterized as a potent vasoconstrictor peptide secreted by vascular endothelial cells. It possesses a wide range of biological activities within the cardiovascular system and in other organs, including the brain. Also secreted by endothelial cells, nitric oxide (NO), has recently been identified as a relaxing factor, as well as a pleiotropic mediator, second messenger, immune defence molecule, and neurotransmitter.

Catecholamines stimulate MHC class I, class II, and invariant chain gene expression in brain endothelium through different mechanisms.

Bovine brain microvessel endothelial cells in primary culture retain a differentiated phenotype reminiscent of the in vivo blood-brain barrier endothelium. The IFN-gamma-induced surface expression of MHC class II molecules on those cells is stimulated by catecholamines through a cAMP-independent mechanism. We report that both the induction of MHC class II molecule expression by IFN-gamma and its potentiation by isoproterenol, a catecholamine analog, are preceded by increases of steady-state levels of the corresponding mRNA.