Inactivation of BACE1 increases expression of endothelial nitric oxide synthase in cerebrovascular endothelium.

ABSTRACT: Cerebrovascular effects of β-site amyloid precursor protein-cleaving enzyme 1 (BACE1) inactivation have not been systematically studied. In the present study we employed cultured human brain microvascular endothelial cells (BMECs), BACE1-knockout (BACE1^-/-) mice and conditional (tamoxifen-induced) endothelium-specific BACE1-knockout (eBACE1^-/-) mice to determine effect of BACE1 inhibition on expression and function of endothelial nitric oxide synthase (eNOS). Deletion of BACE1 caused upregulation of eNOS and glypican-1 (GPC1) in human BMECs treated with BACE1-siRNA, and cerebral microvessels of male BACE1^-/- mice and male eBACE1^-/- mice. In addition, BACE1siRNA treatment increased NO production in human BMECs. These effects appeared to be indepen

SUBMITTER: He T 

PROVIDER: S-EPMC9536128 | biostudies-literature | 2022 Oct

REPOSITORIES: biostudies-literature