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The mechanism of cholesterylester accumulation in smooth muscle cells was investigated.
2
When membrane cholesterol levels are low, absorption of cholesterol effectively drives cholesterylester hydrolysis.
3
This difference is consistent with reports of the nonendocytotic selective uptake of HDL-associated cholesterylester.
4
Unexpectedly, cholesterylester transfer protein was not required to determine the human-like cholesterol lipoprotein profile.
5
Our results demonstrate that lysosomal hydrolysis of cholesterylester is independent of the presence of extracellular acceptors.
6
We show that net hydrolysis of cholesterylester is coupled to the transfer of cholesterol to membranes.
7
These results show that aortic smooth muscle cells in cooperation with macrophages can accumulate cholesterylester from beta-VLDL.
8
In endosomes and lysosomes cholesterylester is hydrolyzed by acidic cholesterylester hydrolase producing cholesterol and fatty acids.
9
Here, we have studied endosomal and lysosomal cholesterylester metabolism in cultured mouse macrophages and with cell-free extracts.
10
J774 and elicited mouse peritoneal macrophages were loaded with cholesterylester within lysosomes through phagocytosis of sonicated lipid droplets.
11
Human plasma lipid transfer protein ( cholesterylester transfer protein) has been characterized for its solution and surface properties.
12
The formation of cholesterol monohydrate crystals was observed in cholesterylester-loaded macrophages after a 48-h incubation by polarizing light microscopy.
13
A reduction in cholesterylester transfer protein (CETP) activity has been advanced to explain most lipid-modulating effects of NA.
14
Additional Mendelian randomization analysis failed to clarify the involvement of cholesterylester transfer protein in alcohol-related changes in lipoprotein cholesterol levels.
15
Electron microscopy and acid phosphatase cytochemistry of lysosomes in cholesterylester-loaded cells confirmed that cholesterol crystal formation occurred within lipid-loaded lysosomes.
16
Thus, the present data do not rule out the involvement of direct HDL-cell interaction in the selective uptake of HDL cholesterylester.