Cholesterol depletion inhibits the degradation of amyloid beta-peptide in rat pheochromocytoma (PC12) cells.
Amyloid beta-peptide (Abeta) is a very important pathogenic factor for Alzheimer's disease (AD). It is a constitutive product of cellular metabolism and occurs in normal biological fluids, such as CSF and plasma. As the steady state levels of all peptides in vivo are a direct consequence of the balance between their anabolism and catabolism, peptide accumulation can arise not only from increased production but also from decreased breakdown. Although increasing evidence indicates that cholesterol is a risk factor for AD development, the exact mechanisms of cholesterol on Abeta metabolism or deposition have remained unclear. Here, we focus our attention on the effect of cholesterol depletion on the degradation of Abeta1-40. Cholesterol depletion of cultured rat pheochromocytoma (PC12) cells was achieved by methyl-beta-cyclodextrin (MbetaCD) extraction. It was found that cholesterol depletion by MbetaCD extraction can suppress Abeta degradation in PC12 cells.
Sun
Zhen-Xiao
ZX
Department of Biological Science and Biotechnology, State Key Laboratory of Biomembrane, Tsinghua University, Beijing 100084, PR China.
Zhou
Qing-Hua
QH
Sui
Sen-Fang
SF
D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000818:Animals; D001673:Biodegradation, Environmental; D002784:Cholesterol / Q000172:deficiency*; D016716:PC12 Cells; D051381:Rats; D047392:beta-Cyclodextrins / Q000494:pharmacology*
D016229:Amyloid beta-Peptides; D047392:beta-Cyclodextrins; C108732:methyl-beta-cyclodextrin; D002784:Cholesterol