Alteration of high density lipoprotein subfraction distribution with induction of serum amyloid A protein (SAA) in the nonhuman primate.
Overnight chair restraint results in a dramatic increase in serum amyloid A protein (apoSAA) of nonhuman primate high density lipoprotein (HDL). To determine whether apoSAA induction resulted in a displacement of indigenous HDL protein or a change in the subfraction distribution of HDL, we analyzed the characteristics of HDL subfractions in eight vervet monkeys before and 24 hr after apoSAA induction. Blood was taken from each animal before and after chair restraint to induce apoSAA. HDL was isolated from the plasma by ultracentrifugation and agarose column chromatography. The isolated HDL was subfractionated by density gradient centrifugation and five resulting subfractions were analyzed for protein and lipid content. With apoSAA induction there was a significant increase in d less than 1.09 g/ml protein, phospholipid, and free and esterified cholesterol which resulted in a 44% increase in the total mass of this subfraction. Concomitantly, there was a significant decrease in d 1.10-1.11 g/ml protein, total cholesterol, and cholesteryl ester, which resulted in a 16% decrease in the total mass of the subfraction. The response of the d 1.10-1.11 and d greater than 1.12 g/ml subfraction protein, cholesterol, and phospholipid concentrations to chair restraint for individual animals was directly proportional to their plasma HDL concentrations. Although there was a change in the HDL subfraction concentrations after chair restraint, there was no change in the lipid composition of the HDL subfractions nor in the total amount of HDL protein. However, the apoSAA/A-I ratio was significantly increased with induction while the apoA-II + C's/A-I ratio remained unchanged. The apoSAA/A-I ratio progressively increased with the density of the HDL subfraction. The protein composition of the d greater than 1.12 g/ml subfraction was changed from an average of three apoA-I and two apoA-II (or C's) molecules per particle to an average of two apoA-I, one apoA-II (or C's), and three or four apoSAA molecules per particle after chair restraint. Thus, apoSAA was predominantly associated with the denser HDL subfractions even though the lighter HDL subfractions were the most responsive in terms of changes in concentration. These data suggest that chair restraint of nonhuman primates induces apoSAA which displaces apoA-I and apoA-II or C's from HDL without altering the overall lipid and protein composition of the particle. In addition, chair restraint alters the concentration of HDL subfractions in ways that may be independent of apoSAA induction.
D000682:Amyloid / Q000494:pharmacology*; D000818:Animals; D016632:Apolipoprotein A-I; D016633:Apolipoprotein A-II; D001054:Apolipoproteins A / Q000032:analysis; D001056:Apolipoproteins C / Q000032:analysis; D002499:Centrifugation, Density Gradient; D002521:Cercopithecus / Q000378:metabolism*; D002522:Chlorocebus aethiops / Q000378:metabolism*; D004032:Diet; D004591:Electrophoresis, Polyacrylamide Gel; D008075:Lipoproteins, HDL / Q000378:metabolism*; D008297:Male; D000685:Serum Amyloid A Protein / Q000494:pharmacology*
D000682:Amyloid; D016632:Apolipoprotein A-I; D016633:Apolipoprotein A-II; D001054:Apolipoproteins A; D001056:Apolipoproteins C; D008075:Lipoproteins, HDL; D000685:Serum Amyloid A Protein