Vascular endothelial cells promote cortical neurite outgrowth via an integrin β3-dependent mechanism.

Biochem Biophys Res Commun

Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan; Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency, 5, Sanbancho, Chiyoda-ku, Tokyo 102-0075, Japan. Electronic address:

Published: July 2014

The interaction of neurons with their non-neuronal milieu plays a crucial role in the formation of neural networks, and wide variety of cell-contact-dependent signals that promote neurite elongation have been identified. In this study, we found that vascular endothelial cells promote neurite elongation in an integrin β3-dependent manner. Vascular endothelial cells from the cerebral cortex promoted neurite elongation of cortical neurons in a cell contact-dependent manner. This effect was mediated by arginine-glycine-aspartic acid (RGD), a major recognition sequence for integrins. Pharmacological blockade of integrin β3 abolished the neurite elongation effect induced by the endothelial cells. Immunocytochemical analysis revealed that integrin β3 was expressed on cultured cortical neurons. These results demonstrate that the neurite elongation promoted by vascular endothelial cells requires integrin β3. Vascular endothelial cells may therefore play a role in the development and repair of neural networks in the central nervous system.

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http://dx.doi.org/10.1016/j.bbrc.2014.06.012DOI Listing

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