title: SR-BI selective lipid uptake: subsequent metabolism of acute phase HDL.
abstract: OBJECTIVE
  The purpose of this study was to investigate the interaction of SAA and SR-BI in remodeling of acute phase HDL (AP HDL).
  
  
  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.
authors.affiliation: Graduate Center for Nutritional Science, University of Kentucky Medical Center, Lexington, USA. mdebeer@uky.edu
authors.forename: Maria C
authors.initials: MC
authors.lastname: de Beer
authors.forename: Nancy R
authors.initials: NR
authors.lastname: Webb
authors.forename: Nathan L
authors.initials: NL
authors.lastname: Whitaker
authors.forename: Joanne M
authors.initials: JM
authors.lastname: Wroblewski
authors.forename: Anisa
authors.initials: A
authors.lastname: Jahangiri
authors.forename: Deneys R
authors.initials: DR
authors.lastname: van der Westhuyzen
authors.forename: Frederick C
authors.initials: FC
authors.lastname: de Beer
mesh_terms: D000210:Acute-Phase Reaction / Q000139:chemically induced / Q000378:metabolism*; D000256:Adenoviridae / Q000235:genetics; D000818:Animals; D016632:Apolipoprotein A-I / Q000172:deficiency / Q000235:genetics; D016633:Apolipoprotein A-II / Q000378:metabolism; D001692:Biological Transport; D004195:Disease Models, Animal; D005822:Genetic Vectors; D008070:Lipopolysaccharides; D008075:Lipoproteins, HDL / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D010316:Particle Size; D051122:Scavenger Receptors, Class B / Q000235:genetics / Q000378:metabolism*; D000685:Serum Amyloid A Protein / Q000235:genetics / Q000378:metabolism; D013997:Time Factors
chemical_list: D016632:Apolipoprotein A-I; D016633:Apolipoprotein A-II; D008070:Lipopolysaccharides; D008075:Lipoproteins, HDL; C454739:Scarb1 protein, mouse; D051122:Scavenger Receptors, Class B; D000685:Serum Amyloid A Protein; C440499:lipopolysaccharide, Escherichia coli O111 B4