%0 Journal Article
%T Cholesterol Potentiates <i>¦Â</i>-Amyloid Genesis in Cultured Human Umbilical Vein Endothelial Cells
%A Guozhi Huang
%A Zhiqin Xue
%A Xia Hu
%A Lily Wan
%A Jianming Li
%A Yan Cai
%A Peter R. Patrylo
%A Xuegang Luo
%A Aihua Pan
%A Xiao-Xin Yan
%J Advances in Alzheimer's Disease
%P 23-34
%@ 2169-2467
%D 2016
%I Scientific Research Publishing
%R 10.4236/aad.2016.52002
%X Cerebral Amyloid Angiopathy (CAA) occurs commonly among the elderly and almost invariably in patients with Alzheimer¡¯s Disease (AD). The <i>¦Â</i>-amyloid peptides (A<i>¦Â</i>) are produced via the amy-loidogenic processing of <i>¦Â</i>-Amyloid Precursor Protein (APP) by <i>¦Â</i>-secretase-1 (BACE1) and <i>¦Ã</i>-   secretase. Vascular endothelial cells are lately shown to possess the molecular machinery of A<i>¦Â</i> production, which might participate in the development of CAA. Hypercholesterolemia is considered a risk factor for AD, whereas less is known if cholesterol may modulate endothelial A<i>¦Â</i> production. In the present study we verified the amyloidogenic capability of Human Umbilical Vein Endothelial Cells (HUVECs) in vitro and explored the effect of cholesterol exposure on their amy-loidogenic potential. Cholesterol treatments at 12.5 and 25 mg/dL significantly elevated APP, BACE1 and APP <i>¦Â</i>-CTF protein levels and <i>¦Â</i>-site APP cleavage activity in cell lysates, and A<i>¦Â</i>40 levels in culture medium. However, coincubation with cholesterol at 50 and 100 mg/dL attenuated the viability of the cultured cells and diminished their amyloidogenic capability. These findings suggest that high cholesterol exposure is stressful to vascular endothelial cells, and at a certain dosage range can promote an amyloidogenic response in these cells.
%K Aging
%K Alzheimer¡¯s Disease
%K Cholesterol
%K Neurodegeneration
%K Vascular Dementia
%U http://www.scirp.org/journal/PaperInformation.aspx?PaperID=67101