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expression and
apolipoprotein A-I promoter activity in Hep G2 cells
1 Department of Nutrition and Food Science, University of Maryland, College Park, 20742; and 2 Nutrient Requirements and Functions Laboratory, Beltsville Human Nutrition Research Center, Agricultural Research Service, U.S. Department of Agriculture, Beltsville, Maryland 20705
We examined the influence of
zinc status on expression of certain transcription factors involved in
regulation of apolipoprotein A-I (apoAI) expression in human
hepatoblastoma Hep G2 cells. A low zinc basal medium (zinc deficient,
ZD) consisting of DMEM and 10% Chelex100-treated fetal bovine serum
was used to deplete cellular zinc over one passage. Cells were also
cultured for one passage in medium supplemented with 0.4 (ZD0.4), 4.0 (zinc normal, ZN), 16.0 (zinc adequate, ZA), or 32.0 µM zinc (zinc
supplemented, ZS). Compared with ZN cells, cellular zinc levels were 43 and 31% lower in ZD and ZD0.4 cells but 70 and 146% higher in ZA and ZS cells, respectively. Supplementation of 0.4 µM zinc significantly increased DNA contents per plate, from 65% in ZD cells to 83% in
ZD0.4 cells compared with ZN cells. Addition of >4 µM zinc in medium
did not further increase DNA contents. The proportion of cells in
G1/S and S phase was about fourfold higher and threefold lower, respectively, in ZD cells compared with ZN and other groups. Nuclear Egr-1 protein was markedly decreased in ZD and ZD0.4 cells. Moreover, hepatocyte nuclear factor (HNF)-3
was severely degraded in
ZD and ZD0.4 cells. In contrast, HNF-4
remained stable in all groups
and was not significantly lower in ZD and ZD0.4 cells. Furthermore,
downregulation of trans-acting factor Egr-1 and cleavage of
HNF-3 were associated with reduction of apoAI promoter activity in
zinc-deficient Hep G2 cells. Thus zinc is critical in transcriptional regulation of apoAI gene expression in hepatocytes.
hepatocyte nuclear factor-4; cell cycle; zinc supplementation; G1/S arrest
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