JACC
HOME SUBSCRIPTIONS CURRENT ISSUE PAST ISSUES CARDIOSOURCE SEARCH HELP FEEDBACK
QUICK SEARCH:   [advanced]


     

J Am Coll Cardiol, 2005; 46:1792-1798, doi:10.1016/j.jacc.2005.06.080 (Published online 18 October 2005).
© 2005 by the American College of Cardiology Foundation
This Article
Right arrow Abstract Freely available
Right arrow Full Text
Right arrow Full Text (PDF)
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 ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (37)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ansell, B. J.
Right arrow Articles by Fonarow, G. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ansell, B. J.
Right arrow Articles by Fonarow, G. C.

High-Density Lipoprotein Function

Recent Advances

Benjamin J. Ansell, MD, FACC, Karol E. Watson, MD, PhD, Alan M. Fogelman, MD, FACC, Mohamad Navab, PhD and Gregg C. Fonarow, MD, FACC*

Atherosclerosis Research Unit, Division of Cardiology, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California.



View larger version (92K):

[in a new window]
  		Figure 1 Model of bidirectional conversion of high-density lipoprotein (HDL) from anti-inflammatory (a) to proinflammatory (b), and the role of myeloperoxidase in catalyzing oxidative modification of HDL, rendering it unable to effect adenosine triphosphate-binding cassette transporter A1-mediated cholesterol transport, modified from Fogelman et al. (2). In association with these changes, apolipoprotein A-1 (apoA-1) and paraoxonase levels decrease, while proinflammatory factors such as lipid oxidation products increase.

 


View larger version (41K):

[in a new window]
  		Figure 2 Enzymatic and protein changes within high-density lipoprotein (HDL) during an acute phase reaction. Serum amyloid A (SAA), apolipoprotein J (J), and secretory nonpancreatic phospholipase A2 (sPLA2) are present at higher serum concentrations and incorporate into HDL, while the HDL components apolipoprotein A-I (A-I), paraoxonase 1 (PON1), platelet activating factor acyl hydrolase (PAF-AH), cholesteryl ester transfer protein (CETP), lecithin:cholesterol acyltransferase (LCAT), and phospholipid transfer protein (PLTP) all decrease in concentration within HDL. High-density lipoprotein phospholipid content also falls, along with a reduction in cholesterol esters and an increase in triglycerides, free fatty acids, and free cholesterol. A-II = apolipoprotein A-II. From Rohrer et al. (31).

 


View larger version (19K):

[in a new window]
  		Figure 3 (A) High-density lipoprotein (HDL) inflammatory index (mean ± SD), as determined by comparing low-density-lipoprotein-induced monocyte migration in an artery wall cell co-culture assay with HDL from healthy controls, HDL from patients with coronary heart disease/risk equivalents before/after simvastatin 40 mg/day for six weeks, and no HDL (defined as an inflammatory index of 1.0). From Navab et al. (4). (B) High-density lipoprotein inflammatory index from the same subjects, using a cell-free assay.

 




HOME SUBSCRIPTIONS CURRENT ISSUE PAST ISSUES CARDIOSOURCE SEARCH HELP FEEDBACK
Copyright © 2005 by the American College of Cardiology Foundation.