Effect of low density lipoproteins, high density lipoproteins, and cholesterol on apolipoprotein AI mRNA in Hep G2 cells
JC Monge, JM Hoeg, SW Law, HB Brewer jr - FEBS letters, 1989 - Elsevier
JC Monge, JM Hoeg, SW Law, HB Brewer jr
FEBS letters, 1989•ElsevierWe have utilized the human hepatocellular carcinoma cell line, Hep G2, to study the effects
of low density lipoproteins (LDL), high density lipoproteins (HDL), and free cholesterol on
apolipoprotein (apo) AI mRNA levels. Incubation of the Hep G2 cells with LDL and free
cholesterol led to a significant increase in the cellular content of cholesterol without any
effect on the yield of total RNA or in the cellular protein content. Our studies established that
incubation with LDL or free cholesterol increased the relative levels of apoA-I mRNA in the …
of low density lipoproteins (LDL), high density lipoproteins (HDL), and free cholesterol on
apolipoprotein (apo) AI mRNA levels. Incubation of the Hep G2 cells with LDL and free
cholesterol led to a significant increase in the cellular content of cholesterol without any
effect on the yield of total RNA or in the cellular protein content. Our studies established that
incubation with LDL or free cholesterol increased the relative levels of apoA-I mRNA in the …
Abstract
We have utilized the human hepatocellular carcinoma cell line, Hep G2, to study the effects of low density lipoproteins (LDL), high density lipoproteins (HDL), and free cholesterol on apolipoprotein (apo) A-I mRNA levels. Incubation of the Hep G2 cells with LDL and free cholesterol led to a significant increase in the cellular content of cholesterol without any effect on the yield of total RNA or in the cellular protein content. Our studies established that incubation with LDL or free cholesterol increased the relative levels of apoA-I mRNA in the Hep G2 cells. In contrast with cholesterol loading, HDL had the effect of lowering the levels of apoA-I mRNA. These results indicate the LDL and HDL pathways as well as intracellular cholesterol may be important in apoA-I gene expression and regulation.
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