HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Renier, G. Articles by Mikhail, R. Search for Related Content PubMed PubMed Citation Articles by Renier, G. Articles by Mikhail, R. Social Bookmarking                      What's this?

Journal of Lipid Research, Vol 37, 799-809, Copyright © 1996 by Lipid Research, Inc.

ARTICLES

Role of oxidant injury on macrophage lipoprotein lipase (LPL) production and sensitivity to LPL

G Renier, AC Desfaits, A Lambert and R Mikhail
Department of Nutrition, Notre-Dame Hospital Research Center, University of Montreal, Quebec, Canada.

We investigated, in the present study, the role of reactive oxygen intermediates (ROI) in the control of macrophage lipoprotein lipase (LPL) secretion. Exposure of murine macrophages to increasing concentrations of hydrogen peroxide (H2O2) resulted in enhanced basal LPL production and mRNA levels. The increase of LPL production was reduced in the presence of antioxidants. Oxidant stress also modulated the regulation of macrophage LPL production by tumor necrosis factor alpha (TNF alpha). While antioxidants accentuated the inhibition of LPL by TNF alpha, addition of H2O2 significantly attenuated TNF alpha- induced LPL inhibition. As LPL has been shown to induce macrophage TNF alpha release, the effect of reactive oxygen species on LPL-induced TNF alpha production was also examined. Simultaneous treatment of macrophages with LPL and H2O2 or pretreatment of macrophages with H2O2 prior to LPL stimulation decreased the LPL-induced TNF alpha release by macrophages to the same extent. Under these experimental conditions, LPL binding to macrophages was markedly decreased. These data indicate that ROI are effective enhancers of macrophage LPL production and modulate macrophage response to LPL. These effects may represent additional mechanisms through which oxidant stress may participate to the development of atherosclerosis.
CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				F. Maingrette, L. Li, and G. Renier C-reactive protein enhances macrophage lipoprotein lipase expression J. Lipid Res., September 1, 2008; 49(9): 1926 - 1935. [Abstract] [Full Text] [PDF]

				M.-C. Beauchamp, S.-E. Michaud, L. Li, M. R. Sartippour, and G. Renier Advanced glycation end products potentiate the stimulatory effect of glucose on macrophage lipoprotein lipase expression J. Lipid Res., September 1, 2004; 45(9): 1749 - 1757. [Abstract] [Full Text] [PDF]

				O. Serri, L. Li, F. Maingrette, N. Jaffry, and G. Renier Enhanced Lipoprotein Lipase Secretion and Foam Cell Formation by Macrophages of Patients with Growth Hormone Deficiency: Possible Contribution to Increased Risk of Atherogenesis? J. Clin. Endocrinol. Metab., February 1, 2004; 89(2): 979 - 985. [Abstract] [Full Text] [PDF]

				J. R Mead and D. P Ramji The pivotal role of lipoprotein lipase in atherosclerosis Cardiovasc Res, August 1, 2002; 55(2): 261 - 269. [Full Text] [PDF]

				M. Lucas, P.-H. Iverius, D. K. Strickland, and T. Mazzone Lipoprotein Lipase Reduces Secretion of Apolipoprotein E from Macrophages J. Biol. Chem., May 16, 1997; 272(20): 13000 - 13005. [Abstract] [Full Text] [PDF]