Modulation of cellular adhesion in bovine brain microvessel endothelial cells by a decapeptide

摘要: Abstract The importance of cell adhesion molecules in maintaining the cellular integrity endothelial layer is well recognized, yet their exact participation regulating blood–brain barrier (BBB) poorly understood. Both Ca2+-dependent and Ca2+-independent are found cells. In this study, we used immunofluorescence, ELISA, Western blot assay to identify a molecule, E-cadherin, bovine brain microvessel cells (BBMECs). Monoclonal anti-E-cadherin antibody specifically interacted with cultured BBMECs decorated junctions series punctate fluorescence spots as seen by indirect immunofluorescence using confocal microscope. intensity these increased after brief treatment hIFN-γ or CPT-cAMP. extract BBMECs, 120 kDa protein was immunoprecipitated antibody. did not react anti-N-cadherin antibody, but recognized FITC-labeled LRAHAVDVNG-NH2, decapeptide generated from EC-1 domain N-cadherin, which lateral margins spots. A concentration-dependent binding also observed flow cytometry assay. dissociated trypsin plus Ca2+ were able reaggregate only presence Ca2+. However, such cell-cell aggregations prevented either medium. These results confirm that possess distinct mechanism can be modulated decapeptide. This modulation thought-provoking for creating channels paracellular drug delivery across BBB.