Cholesterol overload often happens to adult neurons, because they primarily rely on exogenous cholesterol, whereas astrocytes produce cholesterol in excess to satisfy adult neurons' functional needs.
For those aiming for complete cholesterol overload there were great dessert picks: a creamy cheesecake, whipped cream-topped Key lime pie, rich chocolate velvet cake and the even better Godiva hot chocolate cake with a runny center.
Moreover, Rh2-induced Fas oligomerization was abolished following cholesterol overloading, and Rh2-induced apoptosis was inhibited following treatment with siRNA for Fas.
Since cholesterol overloading, which fortifies lipid rafts, prevented an increase in Rh2-induced membrane fluidity, caveolin-1 internalization and apoptosis, lipid rafts appear to be essential for Rh2-induced apoptosis.
The effectiveness of the MβCD depletion and cholesterol overload was confirmed (40% reduction in total cholesterol after MβCD depletion; 250%, ±13% increase after overload; see [51]).
Finally, to further investigate the consequences of late endosomal cholesterol overload, we made use of Vesicular Stomatitis Virus (VSV), which infects cells from endosomes.
The intracellular trafficking of sphingolipid analogs is also known to be affected by cholesterol overloading of mammalian fibroblasts and neurons [12].
In summary, it appears that SBD trafficking is strongly influenced by cellular cholesterol levels, especially cholesterol overload, and this may reflect an underlying event involving the trafficking of its glycosphingolipid partner(s).
Under cholesterol overload (shown by filipin staining in and around endolysosomal compartments; fig. 9C) SBD was actually endocytosed more readily (quantification in fig. S6), but trafficking was strongly perturbed.
This indicates that neither depletion of total cellular cholesterol levels nor cholesterol overload are a likely cause of cell death observed in breast cancer cell lines, in particular because activation of SREBP-2 was also observed in the relatively resistant MCF10A cells (Figure S2).
Uptake of modified lipoproteins by macrophages in the vasculature leads to cholesterol overload and formation of atherogenic foam cells [ 13].
