Journal
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
Volume 29, Issue 9, Pages 1298-1303Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/ATVBAHA.109.186502
Keywords
SAA; HDL; inflammation; SR-BI; metabolism
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Funding
- NIH [PO1 HL086670]
- VA Merit Review Funds
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Objective-The purpose of this study was to investigate the interaction of SAA and SR-BI in remodeling of acute phase HDL (AP HDL). Methods and Results-We used SAA and SR-BI adenoviral vector expression models to study the interaction between these entities. SR-BI processing of mouse AP HDL generated progressively smaller discreet HDL particles with distinct apolipoprotein compositions. SR-BI actions segregated apolipoproteins with the smallest particles containing only apoA-I. Larger remnants contained apoA-I, apoA-II, and SAA. Small apoA- I only particles failed to associate with preformed HDL, whereas larger remnants readily did. The presence of SAA on SR-BI-processed HDL particles propelled apoA- I to a small lipid-poor form and accelerated apoA- I catabolism. Conclusions-Data indicate that after core and surface HDL lipid perturbation by SR-BI, SAA propels apoA- I to a small lipid-poor form while accelerating HDL metabolism. (Arterioscler Thromb Vasc Biol. 2009;29:1298-1303.)
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