Parks J S, Rudel L L
J Lipid Res. 1985 Jan;26(1):82-91.
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.
夜间使用椅子约束导致非人类灵长类动物高密度脂蛋白（HDL）的血清淀粉样蛋白A（apoSAA）显著增加。为了确定apoSAA的诱导是否导致了天然HDL蛋白的置换或HDL亚组分分布的变化，我们分析了八只黑长尾猴在apoSAA诱导前和诱导后24小时的HDL亚组分特征。在使用椅子约束诱导apoSAA前后，从每只动物采集血液。通过超速离心和琼脂糖柱色谱从血浆中分离HDL。通过密度梯度离心对分离出的HDL进行亚组分分离，并对得到的五个亚组分的蛋白质和脂质含量进行分析。随着apoSAA的诱导，密度小于1.09 g/ml的蛋白质、磷脂以及游离和酯化胆固醇显著增加，导致该亚组分的总质量增加了44%。与此同时，密度为1.10 - 1.11 g/ml的蛋白质、总胆固醇和胆固醇酯显著减少，导致该亚组分的总质量减少了16%。对于个体动物，密度为1.10 - 1.11 g/ml和密度大于1.12 g/ml的亚组分蛋白质、胆固醇和磷脂浓度对椅子约束的反应与它们的血浆HDL浓度成正比。尽管椅子约束后HDL亚组分浓度发生了变化，但HDL亚组分的脂质组成以及HDL蛋白总量均未改变。然而，诱导后apoSAA/A-I比值显著增加，而apoA-II + C's/A-I比值保持不变。apoSAA/A-I比值随着HDL亚组分的密度逐渐增加。密度大于1.12 g/ml的亚组分的蛋白质组成从每个颗粒平均三个apoA-I和两个apoA-II（或C's）分子变为椅子约束后每个颗粒平均两个apoA-I、一个apoA-II（或C's）以及三个或四个apoSAA分子。因此，尽管较轻的HDL亚组分在浓度变化方面反应最灵敏，但apoSAA主要与密度较大的HDL亚组分相关。这些数据表明，对非人类灵长类动物进行椅子约束会诱导apoSAA，其从HDL中置换apoA-I和apoA-II或C's，而不改变颗粒的整体脂质和蛋白质组成。此外，椅子约束以可能独立于apoSAA诱导的方式改变HDL亚组分的浓度。
