HMG CoA Reductase and LDL Receptor Genes Are Regulated Differently by 15-Ketosterols in Hep G2 Cells

1999 ◽  
Vol 259 (3) ◽  
pp. 688-694 ◽  
Author(s):  
Anastassia F. Kisseleva ◽  
Ludmila E. Goryunova ◽  
Richard Planells ◽  
Huguette Lafont ◽  
Christian Alquier
Keyword(s):  
Ldl Receptor ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
Hmg Coa Reductase ◽  
G2 Cells ◽  
Coa Reductase

Effect of ketoconazole on cholesterol synthesis and on HMG-COA reductase and LDL-receptor activities in Hep G2 cells

1987 ◽  
Vol 36 (8) ◽  
pp. 1245-1249 ◽  
Author(s):  
Herman Jan Kempen ◽  
Kees Van Son ◽  
Louis H. Cohen ◽  
Marieke Griffioen ◽  
Hans Verboom ◽  
...  
Keyword(s):  
Cholesterol Synthesis ◽  
Ldl Receptor ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
Hmg Coa Reductase ◽  
G2 Cells ◽  
Coa Reductase

2.P.11 Effects of atorvastatin on intracellular levels and stability of apolipoprotein B and HMG-CoA reductase in Hep G2 cells

1997 ◽  
Vol 134 (1-2) ◽  
pp. 119
Author(s):  
K. Adeli ◽  
T. Romain ◽  
A. Mohammadi ◽  
R.S. Newton ◽  
R. Cheung ◽  
...  
Keyword(s):  
Apolipoprotein B ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
Hmg Coa Reductase ◽  
G2 Cells ◽  
Coa Reductase

scholarly journals Regulation of cholesterol biosynthesis and metabolismin Hep G2 cells by δ8(14)-15-ketoergostane derivatives

2010 ◽  
Vol 56 (5) ◽  
pp. 576-586
Author(s):  
A.R. Mehtiev ◽  
V.I. Fedchenko ◽  
Ya.V. Tkachev ◽  
V.P. Timofeev ◽  
A.Yu. Misharin
Keyword(s):  
Cholesterol Biosynthesis ◽  
Mrna Level ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
Hmg Coa Reductase ◽  
Side Chain Conformation ◽  
Genes Expression ◽  
G2 Cells ◽  
Coa Reductase ◽  
The Comparative Study

The comparative study of effects of 5α-cholest-8(14)-en-15-on-3β-ol (I), (22E)-5α-ergosta-8(14),22-dien-15-on-3β-ol (II), (22S,23S)-22,23-oxido-5α-ergost-8(14)-en-15-on-3β-ol (III) and (22R,23R)-22,23-oxido-5α-ergost-8(14)-en-15-on-3β-ol (IV) on HMG-CoA reductase, CYP27A1 and CYP3A4 genes expression in Hep G2 cells was performed. In the contrast to 15-ketocholestane derivative (I), 15-ketoergostane derivatives (II - IV) decreased the HMG- CoA reductase mRNA level; (22R,23R)-22,23-oxido-5α-ergost-8(14)-en-15-on-3β-ol (IV) significantly increased CYP3A4 mRNA level (320% from control). Ketosterol (II) was found to be a more potent inhibitor of cholesterol biosynthesis in Hep G2 cells at a prolong incubation, compared with ketosterol (I). The side chain conformation of compounds (I) - (IV) was evaluated by computational modeling; the correlation between biological activity of these compounds and conformational flexibility of their side chains was found. The results obtained indicated that Δ8(14)-15-ketoergostane derivatives may be used as a sterol biosynthesis and metabolism regulators in liver cells.

Effect of ethanol on cell growth and cholesterol metabolism in cultured Hep G2 cells

2003 ◽  
Vol 81 (6) ◽  
pp. 379-386 ◽  
Author(s):  
Mónica P Polo ◽  
Margarita G de Bravo ◽  
María JT de Alaniz
Keyword(s):  
Growth Rate ◽  
Cell Growth ◽  
Culture Medium ◽  
Cholesterol Metabolism ◽  
Reductase Activity ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
Hmg Coa Reductase ◽  
G2 Cells ◽  
Coa Reductase

The Hep G2 human hepatoma cell line has been recognized as an excellent in vitro human model system. For this reason, this line was used to study the effect of ethanol on HMG-CoA reductase activity concerning cell growth and cholesterol metabolism. Cells were incubated in ethanol-containing medium (0–400 mmol/L) for up to 102 h. Ethanol caused an inhibition in the growth rate and in HMG-CoA reductase activity that could be reverted by the removal of ethanol from the culture medium, indicating no cellular damage. These changes cannot be ascribed to the regulatory effect of cholesterol levels, since its content was not modified either in the cells or in the medium. The addition of mevalonate to the culture medium could not revert the growth rate inhibition evoked by ethanol. Moreover, ethanol produced an increment in the cholesterol efflux in [3H]cholesterol-prelabeled cells. We conclude that the decrease in HMG-CoA reductase activity evoked by ethanol treatment on Hep G2 cells would not be the cause but the consequence of the impairment in cellular growth, since this impairment could not be reverted by the addition of mevalonate to the culture medium.Key words: ethanol, cholesterol, HMG-CoA reductase, hepatoma cells, lipid metabolism.

Hep-G2 cells and primary rat hepatocytes differ in their response to inhibitors of HMG-CoA reductase

1990 ◽  
Vol 170 (2) ◽  
pp. 726-734 ◽  
Author(s):  
Mary Kay Shaw ◽  
Roger S. Newton ◽  
Drago R. Sliskovic ◽  
Bruce D. Roth ◽  
Erika Ferguson ◽  
...  
Keyword(s):  
Rat Hepatocytes ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
Hmg Coa Reductase ◽  
Primary Rat Hepatocytes ◽  
G2 Cells ◽  
Coa Reductase

scholarly journals The effect of (−)-hydroxycitrate on the activity of the low-density-lipoprotein receptor and 3-hydroxy-3-methylglutaryl-CoA reductase levels in the human hepatoma cell line Hep G2

1990 ◽  
Vol 272 (1) ◽  
pp. 181-186 ◽  
Author(s):  
T A Berkhout ◽  
L M Havekes ◽  
N J Pearce ◽  
P H E Groot
Keyword(s):  
Low Density Lipoprotein ◽  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Low Density ◽  
Hep G2 ◽  
Atp Citrate Lyase ◽  
Hmg Coa Reductase ◽  
Synthetic Pathway ◽  
Citrate Lyase ◽  
Coa Reductase

(-)-Hydroxycitrate, a potent inhibitor of ATP citrate-lyase, was tested in Hep G2 cells for effects on cholesterol homoeostasis. After 2.5 h and 18 h incubations with (-)-hydroxycitrate at concentrations of 0.5 mM or higher, incorporation of [1,5-14C]citrate into fatty acids and cholesterol was strongly inhibited. This most likely reflects an effective inhibition of ATP citrate-lyase. Cholesterol biosynthesis was decreased to 27% of the control value as measured by incorporations from 3H2O, indicating a decreased flux of carbon units through the cholesterol-synthetic pathway. After 18 h preincubation with 2 mM-(-)-hydroxycitrate, the cellular low-density-lipoprotein (LDL) receptor activity was increased by 50%, as determined by the receptor-mediated association and degradation. Measurements of receptor-mediated binding versus LDL concentration suggests that this increase was due to an increase in the numbers of LDL receptors. Simultaneously, enzyme levels of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase as determined by activity measurements increased 30-fold. Our results suggest that the increases in HMG-CoA reductase and the LDL receptor are initiated by the decreased flux of carbon units in the cholesterol-synthetic pathway, owing to inhibition of ATP citratelyase. A similar induction of HMG-CoA reductase and LDL receptor was also found after preincubations of cells with 0.3 microM-mevinolin, suggesting that the underlying mechanism for this induction is identical for both drugs.

Identification of a functional receptor differing from the LDL receptor that catabolizes chylomicron remnant in Hep G2 cells

1993 ◽  
Vol 104 (1-2) ◽  
pp. 105-115 ◽  
Author(s):  
K HAYASHI ◽  
K NAKASHIMA ◽  
M SAEKI ◽  
H KURUSHIMA ◽  
J KUROKAWA ◽  
...  
Keyword(s):  
Ldl Receptor ◽  
Chylomicron Remnant ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
G2 Cells ◽  
Functional Receptor

Stimulation of LDL receptor activity in Hep-G2 cells by a serum factor(s)

1988 ◽  
Vol 135 (2) ◽  
pp. 213-223 ◽  
Author(s):  
Jeff L. Ellsworth ◽  
Cynthia Brown ◽  
Allen D. Cooper
Keyword(s):  
Ldl Receptor ◽  
Receptor Activity ◽  
Serum Factor ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
G2 Cells ◽  
Stimulation Of
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