Advertisement
J. Lipid Res.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

A more recent version of this article appeared on January 1, 2004

Papers In Press, published online ahead of print October 16, 2003
J. Lipid Res., doi:10.1194/jlr.M300179-JLR200
This Article
Right arrow Full Text (Accepted Manuscript)
Right arrow All Versions of this Article:
M300179-JLR200v1
45/1/106    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lamon-Fava, S.
Right arrow Articles by Micherone, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lamon-Fava, S.
Right arrow Articles by Micherone, D.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Submitted on April 28, 2003
Revised on September 24, 2003
Accepted on October 1, 2003

Regulation of apolipoprotein A-I gene expression: mechanism of action of estrogen and genistein

Stefania Lamon-Fava and Dale Micherone

Lipid Metabolism Laboratory, Tufts University, Boston, MA 02111

Corresponding Author: stefania.lamon-fava{at}tufts.edu

We have previously shown that 17-beta-estradiol (E2) and genistein increase the secretion of apolipoprotein (apo) A-I, the major protein component of high-density lipoproteins, in Hep G2 cells by increasing the transcription of the apo A-I gene. The aim of this study was to elucidate the mechanism mediating the increase in apo A-I gene expression by these compounds. A series of plasmid constructs containing serial deletions of the apo A-I promoter region was generated. The –220 to –148 region of the apo A-I promoter was the smallest region maintaining response to E2 and genistein, and the estrogen antagonist ICI 182,780 completely inhibited the E2 and genistein effect. This region contains a binding site for transcription factors belonging to the steroid/thyroid nuclear receptor superfamily (site A), a binding site for HNF-3b (site B), and two binding sites for Egr-1. Nuclear extracts from cells treated with E2 and genistein showed increased binding to site B and nuclear extracts from genistein-treated cells showed increased binding to Egr-1 oligonucleotide, compared to control cells. An increase in the concentrations of Egr-1 and HNF-3b was observed in nuclear extracts of cells treated with E2 and genistein, compared to control cells. Treatment of Hep G2 cells with a specific inhibitor of MAP kinase, but not with other inhibitors, abolished the stimulation of apo A-I gene expression by E2 and genistein. These results indicate that the MAP kinase pathway is involved in the regulation of apo A-I gene expression by genistein and E2, possibly through downstream regulation of transcription factors binding to the promoter region.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
 Arterioscler. Thromb. Vasc. Bio.Home page
S. Lamon-Fava, M. R. Diffenderfer, P. H. R. Barrett, A. Buchsbaum, M. Nyaku, K. V. Horvath, B. F. Asztalos, S. Otokozawa, M. Ai, N. R. Matthan, et al.
Extended-Release Niacin Alters the Metabolism of Plasma Apolipoprotein (Apo) A-I and ApoB-Containing Lipoproteins
Arterioscler Thromb Vasc Biol, September 1, 2008; 28(9): 1672 - 1678.
[Abstract] [Full Text] [PDF]

Home page
 J. Nutr.Home page
S. Baba, M. Natsume, A. Yasuda, Y. Nakamura, T. Tamura, N. Osakabe, M. Kanegae, and K. Kondo
Plasma LDL and HDL Cholesterol and Oxidized LDL Concentrations Are Altered in Normo- and Hypercholesterolemic Humans after Intake of Different Levels of Cocoa Powder
J. Nutr., June 1, 2007; 137(6): 1436 - 1441.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Clin. Nutr.Home page
S. Baba, N. Osakabe, Y. Kato, M. Natsume, A. Yasuda, T. Kido, K. Fukuda, Y. Muto, and K. Kondo
Continuous intake of polyphenolic compounds containing cocoa powder reduces LDL oxidative susceptibility and has beneficial effects on plasma HDL-cholesterol concentrations in humans
Am. J. Clinical Nutrition, March 1, 2007; 85(3): 709 - 717.
[Abstract] [Full Text] [PDF]

Home page
 Endocr. Rev.Home page
A. D. Mooradian, M. J. Haas, and N. C. W. Wong
The Effect of Select Nutrients on Serum High-Density Lipoprotein Cholesterol and Apolipoprotein A-I Levels
Endocr. Rev., February 1, 2006; 27(1): 2 - 16.
[Abstract] [Full Text] [PDF]

Home page
 Arterioscler. Thromb. Vasc. Bio.Home page
S. Lamon-Fava, B. Postfai, M. Diffenderfer, C. DeLuca, J. O'Connor Jr, F. K. Welty, G. G. Dolnikowski, P. H. R. Barrett, and E. J. Schaefer
Role of the Estrogen and Progestin in Hormonal Replacement Therapy on Apolipoprotein A-I Kinetics in Postmenopausal Women
Arterioscler Thromb Vasc Biol, February 1, 2006; 26(2): 385 - 391.
[Abstract] [Full Text] [PDF]

Home page
 CirculationHome page
D. J. Grainger and P. M. Schofield
Tamoxifen for the Prevention of Myocardial Infarction in Humans: Preclinical and Early Clinical Evidence
Circulation, November 8, 2005; 112(19): 3018 - 3024.
[Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 All ASBMB Journals   Journal of Biological Chemistry 
 Molecular and Cellular Proteomics   ASBMB Today 
Copyright © 2003 by the American Society for Biochemistry and Molecular Biology.
Advertisement
spacer
Advertisement
Advertisement