Abstract
The conversion of cellular prion protein (PrP C) to its protease-resistant isoform is involved in the pathogenesis of prion disease. Although PrP C is a ubiquitous glycoprotein that is present in various cell types, the physiological role of PrP C remains obscure. The present study aimed to determine whether PrP C mediates migration of brain microvascular endothelial cells. Small interfering RNAs (siRNAs) targeting PrP C were transfected into a mouse brain microvascular endothelial cell line (bEND.3 cells). siPrP1, selected among three siRNAs, reduced mRNA and protein levels of PrP C in bEND.3 cells. Cellular migration was evaluated with a scratch-wound assay. siPrP1 suppressed migration without significantly affecting cellular proliferation. This study provides the first evidence that PrP C may be necessary for brain microvascular endothelial cells to migrate into damaged regions in the brain. This function of PrP C in the brain endothelium may be a mechanism by which the neurovascular unit recovers from an injury such as an ischemic insult.
Published Version
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