TY - JOUR
T1 - SR-BI selective lipid uptake
T2 - Subsequent metabolism of acute phase HDL
AU - De Beer, Maria C.
AU - Webb, Nancy R.
AU - Whitaker, Nathan L.
AU - Wroblewski, Joanne M.
AU - Jahangiri, Anisa
AU - Van Der Westhuyzen, Deneys R.
AU - De Beer, Frederick C.
PY - 2009/9
Y1 - 2009/9
N2 - 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.
AB - 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.
KW - HDL
KW - Inflammation
KW - Metabolism
KW - SAA
KW - SR-BI
UR - http://www.scopus.com/inward/record.url?scp=69849111018&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=69849111018&partnerID=8YFLogxK
U2 - 10.1161/ATVBAHA.109.186502
DO - 10.1161/ATVBAHA.109.186502
M3 - Article
C2 - 19304574
AN - SCOPUS:69849111018
SN - 1079-5642
VL - 29
SP - 1298
EP - 1303
JO - Arteriosclerosis, Thrombosis, and Vascular Biology
JF - Arteriosclerosis, Thrombosis, and Vascular Biology
IS - 9
ER -