Intracellular Metabolism of Human Apolipoprotein(a) in Stably Transfected Hep G2 Cells†

Biochemistry ◽  
1998 ◽  
Vol 37 (16) ◽  
pp. 5417-5425 ◽  
Author(s):  
Eva-Maria Lobentanz ◽  
Krisztina Krasznai ◽  
Alexandra Gruber ◽  
Christoph Brunner ◽  
Hans-Joachim Müller ◽  
...  
Keyword(s):  
Hep G2 ◽  
Hep G2 Cells ◽  
Human Apolipoprotein ◽  
Apolipoprotein A ◽  
Intracellular Metabolism ◽  
G2 Cells

Zinc depletion reduced Egr-1 and HNF-3β expression and apolipoprotein A-I promoter activity in Hep G2 cells

2002 ◽  
Vol 283 (2) ◽  
pp. C623-C630 ◽  
Author(s):  
Libin Cui ◽  
Norberta W. Schoene ◽  
Lei Zhu ◽  
Jessica C. Fanzo ◽  
Ali Alshatwi ◽  
...  
Keyword(s):  
Promoter Activity ◽  
Basal Medium ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
Apolipoprotein A ◽  
Zinc Depletion ◽  
Dna Contents ◽  
G2 Cells ◽  
Zinc Levels ◽  
Cellular Zinc

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)-3β was severely degraded in ZD and ZD0.4 cells. In contrast, HNF-4α 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-3β 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.

Dexamethasone increases apolipoprotein A-I concentrations in medium and apolipoprotein A-I mRNA abundance from Hep G2 cells

Metabolism ◽  
1992 ◽  
Vol 41 (10) ◽  
pp. 1075-1080 ◽  
Author(s):  
Vivek K. Varma ◽  
Thuy K. Smith ◽  
Mary Sorci-Thomas ◽  
Walter H. Ettinger
Keyword(s):  
Mrna Abundance ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
Apolipoprotein A ◽  
G2 Cells

Lipid-poor apolipoprotein A-I in Hep G2 cells: formation of lipid-rich particles by incubation with dimyristoylphosphatidylcholine

1987 ◽  
Vol 920 (3) ◽  
pp. 185-194 ◽  
Author(s):  
Trudy M. Forte ◽  
Alex V. Nichols ◽  
Janet Selmek-Halsey ◽  
Lisa Caylor ◽  
Virgie G. Shore
Keyword(s):  
Hep G2 ◽  
Hep G2 Cells ◽  
Apolipoprotein A ◽  
G2 Cells

Transcriptional regulation of apolipoprotein A-I expression in Hep G2 cells by phorbol ester

FEBS Letters ◽  
1995 ◽  
Vol 376 (1-2) ◽  
pp. 99-102 ◽  
Author(s):  
Yves Vandenbrouck ◽  
Gilles Lambert ◽  
Brigitte Janvier ◽  
Delphine Girlich ◽  
Gilbert Bereziat ◽  
...  
Keyword(s):  
Transcriptional Regulation ◽  
Phorbol Ester ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
Apolipoprotein A ◽  
G2 Cells

Apolipoprotein A-I gene expression is regulated by cellular zinc status in Hep G2 cells

1999 ◽  
Vol 277 (3) ◽  
pp. C537-C544 ◽  
Author(s):  
John Y. J. Wu ◽  
Yan Wu ◽  
Scott K. Reaves ◽  
Yi Ran Wang ◽  
Polin P. Lei ◽  
...  
Keyword(s):  
Mrna Levels ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
Normal Cells ◽  
Chelex 100 ◽  
Apolipoprotein A ◽  
G2 Cells ◽  
Zn Status ◽  
Cellular Zinc ◽  
I Gene

The influence of Zn on the expression of the apolipoprotein A-I (apoA-I) gene in Hep G2 cells was examined. Zn depletion was achieved with a low-Zn (ZD) medium prepared from Zn-free growth medium (Opti), a ZD medium containing Chelex 100-extracted fetal bovine serum (CHE), and a medium containing chelator 1,10-phenanthroline (OP). Compared with those for their respective controls, cellular Zn levels were reduced by 55, 48, and 46% and apoA-I mRNA abundances were reduced by 20, 29, and 28% in Opti, CHE, and OP systems, respectively, after one passage in ZD media or 24 h in OP medium. To establish the specificity of Zn treatment, groups of ZD cells were treated with their respective control media for the last 24 h (ZDA) or normal cells were cultured with OP medium supplemented with Zn (OP-Zn). ZDA treatments partially normalized cellular Zn levels in the Opti system and restored or elevated apoA-I mRNA levels in the Opti or CHE system, respectively. Similarly, the OP-Zn treatment restored the cellular Zn and apoA-I mRNA levels. Furthermore, one passage of culture with Zn-supplemented media in both the Opti and CHE systems resulted in higher cellular Zn and apoA-I mRNA levels than those for controls. Most significantly, short-term high-Zn induction to normal cells markedly elevated the cellular Zn (3-fold) and apoA-I mRNA (5-fold) levels. Data derived from this study strongly suggest that the expression of apoA-I is regulated by cellular Zn status.

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