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

J. Biol. Chem., Vol. 278, Issue 42, 40859-40866, October 17, 2003

This Article Full Text Full Text (PDF) All Versions of this Article: 278/42/40859    most recent M306580200v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend 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 Paromov, V. M. Articles by Morton, R. E. Search for Related Content PubMed PubMed Citation Articles by Paromov, V. M. Articles by Morton, R. E. Social Bookmarking                      What's this?

Lipid Transfer Inhibitor Protein Defines the Participation of High Density Lipoprotein Subfractions in Lipid Transfer Reactions Mediated by Cholesterol Ester Transfer Protein (CETP)^*

Viktor M. Paromov and Richard E. Morton 

From the Department of Cell Biology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195

Cholesterol ester transfer protein (CETP) moves triglyceride (TG) and cholesteryl ester (CE) between lipoproteins. CETP has no apparent preference for high (HDL) or low (LDL) density lipoprotein as lipid donor to very low density lipoprotein (VLDL), and the preference for HDL observed in plasma is due to suppression of LDL transfers by lipid transfer inhibitor protein (LTIP). Given the heterogeneity of HDL, and a demonstrated ability of HDL subfractions to bind LTIP, we examined whether LTIP might also control CETP-facilitated lipid flux among HDL subfractions. CETP-mediated CE transfers from [³H]CE VLDL to various lipoproteins, combined on an equal phospholipid basis, ranged 2-fold and followed the order: HDL₃ > LDL > HDL₂. LTIP inhibited VLDL to HDL₂ transfer at one-half the rate of VLDL to LDL. In contrast, VLDL to HDL₃ transfer was stimulated, resulting in a CETP preference for HDL₃ that was 3-fold greater than that for LDL or HDL₂. Long-term mass transfer experiments confirmed these findings and further established that the previously observed stimulation of CETP activity on HDL by LTIP is due solely to its stimulation of transfer activity on HDL₃. TG enrichment of HDL₂, which occurs during the HDL cycle, inhibited CETP activity by 2-fold and LTIP activity was blocked almost completely. This suggests that LTIP keeps lipid transfer activity on HDL₂ low and constant regardless of its TG enrichment status. Overall, these results show that LTIP tailors CETP-mediated remodeling of HDL₃ and HDL₂ particles in subclass-specific ways, strongly implicating LTIP as a regulator of HDL metabolism.

Received for publication, June 20, 2003 , and in revised form, July 28, 2003.

^* This research was supported in part by Grant HL60934 from the NHLBI, National Institutes of Health and Grant 0050075N from the American Heart Association. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed: Dept. of Cell Biology, NC 10, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, OH 44195. Tel.: 216-444-5850; Fax: 216-444-9404; E-mail: mortonr{at}ccf.org.

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

This article has been cited by other articles:

				P. S. Green, T. Vaisar, S. Pennathur, J. J. Kulstad, A. B. Moore, S. Marcovina, J. Brunzell, R. H. Knopp, X.-Q. Zhao, and J. W. Heinecke Combined Statin and Niacin Therapy Remodels the High-Density Lipoprotein Proteome Circulation, September 16, 2008; 118(12): 1259 - 1267. [Abstract] [Full Text] [PDF]

				Y. He, D. J. Greene, M. Kinter, and R. E. Morton Control of cholesteryl ester transfer protein activity by sequestration of lipid transfer inhibitor protein in an inactive complex J. Lipid Res., July 1, 2008; 49(7): 1529 - 1537. [Abstract] [Full Text] [PDF]

				R. E. Morton, H. M. Gnizak, D. J. Greene, K.-H. Cho, and V. M. Paromov Lipid transfer inhibitor protein (apolipoprotein F) concentration in normolipidemic and hyperlipidemic subjects J. Lipid Res., January 1, 2008; 49(1): 127 - 135. [Abstract] [Full Text] [PDF]

				T. Y Li, C. Zhang, F. W Asselbergs, L. Qi, E. Rimm, D. J Hunter, and F. B Hu Interaction between dietary fat intake and the cholesterol ester transfer protein TaqIB polymorphism in relation to HDL-cholesterol concentrations among US diabetic men Am. J. Clinical Nutrition, November 1, 2007; 86(5): 1524 - 1529. [Abstract] [Full Text] [PDF]

				N. Barzilai, G. Atzmon, C. A. Derby, J. M. Bauman, and R. B. Lipton A genotype of exceptional longevity is associated with preservation of cognitive function Neurology, December 26, 2006; 67(12): 2170 - 2175. [Abstract] [Full Text] [PDF]

				J. P. Conway and M. Kinter Dual Role of Peroxiredoxin I in Macrophage-derived Foam Cells J. Biol. Chem., September 22, 2006; 281(38): 27991 - 28001. [Abstract] [Full Text] [PDF]

				J. P. Conway and M. Kinter Proteomic and Transcriptomic Analyses of Macrophages with an Increased Resistance to Oxidized Low Density Lipoprotein (oxLDL)-induced Cytotoxicity Generated by Chronic Exposure to oxLDL Mol. Cell. Proteomics, October 1, 2005; 4(10): 1522 - 1540. [Abstract] [Full Text] [PDF]

				G. F. Lewis and D. J. Rader New Insights Into the Regulation of HDL Metabolism and Reverse Cholesterol Transport Circ. Res., June 24, 2005; 96(12): 1221 - 1232. [Abstract] [Full Text] [PDF]

				R. E. Morton and D. J. Greene CETP and lipid transfer inhibitor protein are uniquely affected by the negative charge density of the lipid and protein domains of LDL J. Lipid Res., December 1, 2003; 44(12): 2287 - 2296. [Abstract] [Full Text] [PDF]