Low density lipoprotein causes general cellular activation with increased phosphatidylinositol turnover and lipoprotein catabolism.
AUTOR(ES)
Block, L H
RESUMO
Low density lipoprotein (LDL), at concentrations high enough for receptor binding but not high enough to saturate the receptor, induces activation of phosphatidylinositol (PtdIns) turnover in a variety of cell types with various biological functions. Using both biochemical and electron microscopic studies, we have shown that blood platelets take up and degrade LDL in a manner reminiscent of phagocytic cell types. The activation of both PtdIns turnover and LDL metabolism is inhibited by high density lipoprotein. Thus, LDL at hormonal concentrations causes general cellular activation. Since all cell types studied responded to LDL with increased PtdIns turnover and uptake of LDL cholesterol, the PtdIns cycle may also be involved in the cellular regulation of LDL cholesterol metabolism.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=279661Documentos Relacionados
- Comparison of glucosylated low density lipoprotein with methylated or cyclohexanedione-treated low density lipoprotein in the measurement of receptor-independent low density lipoprotein catabolism.
- Receptor-mediated Catabolism of Low Density Lipoprotein in Man. QUANTITATION USING GLUCOSYLATED LOW DENSITY LIPOPROTEIN
- Catabolism of Very Low Density Lipoprotein B Apoprotein in Man
- Plasma high density lipoprotein is increased in man when low density lipoprotein (LDL) is lowered by LDL-pheresis.
- Unmodified low density lipoprotein causes cholesteryl ester accumulation in J774 macrophages.