| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Articles in PresS, published online ahead of print April 24, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00308.2001
Submitted on July 6, 2001
Accepted on April 15, 2002
1 Nutrition and Food Science, University of Maryland, College Park, MD
2 Nutrition and Food Science, University of Maryland, College Park, MD, none
* To whom correspondence should be addressed. E-mail: DL165{at}umail.umd.edu.
This study was designed to examine the influence of zinc status on the expression of certain transcription factors known to be involved in the regulation of apolipoprotein A-I
expression in the human hepatoblastoma HepG2 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 media supplemented with 0.4 (ZD0.4), 4.0 (zinc-normal, ZN), 16.0 (zinc-adequate,
ZA), or 32.0 µM of zinc (zinc-supplemented, ZS). As compared to 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 the DNA contents per plate, from 65% in ZD cells to 83% in ZD0.4 cells, as compared to ZN cells. Addition of more than 4 µM of zinc in medium did not further increase the DNA contents. The proportion of cells in G1/S and S phase were about 4-fold higher and 3-fold lower, respectively, in ZD cells as compared to ZN and other groups. Nuclear Egr-1 protein was markedly decreased in the ZD and ZD0.4 cells. Moreover, hepatocyte nuclear factor HNF-3ß was severely degraded in ZD and ZD0.4
cells. In contrast, hepatocyte nuclear factor HNF-4
remained stable in all groups, and was not significantly lower in ZD and ZD0.4 cells. Furthermore, the down-regulation of trans-acting factors Egr-1 and cleavage of HNF-3ß were associated with a reduction of
apoA-I promoter activity in zinc-deficient HepG2 cells. Thus, zinc is critical in the transcriptional regulation of apoA-I gene expression in hepatocytes.
This article has been cited by other articles:
|
|
 |
|
  X. Kang, Z. Song, C. J. McClain, Y. J. Kang, and Z. Zhou Zinc Supplementation Enhances Hepatic Regeneration by Preserving Hepatocyte Nuclear Factor-4{alpha} in Mice Subjected to Long-Term Ethanol Administration Am. J. Pathol., April 1, 2008; 172(4): 916 - 925. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. H. K. Wong, Y. Zhao, N. W. Schoene, C.-T. Han, R. S. M. Shih, and K. Y. Lei Zinc deficiency depresses p21 gene expression: inhibition of cell cycle progression is independent of the decrease in p21 protein level in HepG2 cells Am J Physiol Cell Physiol, June 1, 2007; 292(6): C2175 - C2184. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Z. Zhou, X. Kang, Y. Jiang, Z. Song, W. Feng, C. J. McClain, and Y. J. Kang Preservation of Hepatocyte Nuclear Factor-4{alpha} Is Associated with Zinc Protection Against TNF-{alpha} Hepatotoxicity in Mice Experimental Biology and Medicine, May 1, 2007; 232(5): 622 - 628. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Lamon-Fava and D. Micherone Regulation of apoA-I gene expression: mechanism of action of estrogen and genistein J. Lipid Res., January 1, 2004; 45(1): 106 - 112. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. C. Fanzo, S. K. Reaves, L. Cui, L. Zhu, and K. Y. Lei p53 protein and p21 mRNA levels and caspase-3 activity are altered by zinc status in aortic endothelial cells Am J Physiol Cell Physiol, August 1, 2002; 283(2): C631 - C638. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
