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含血清淀粉样蛋白A的人高密度脂蛋白3。密度、大小及载脂蛋白组成。

Serum amyloid A-containing human high density lipoprotein 3. Density, size, and apolipoprotein composition.

作者信息

Coetzee G A, Strachan A F, van der Westhuyzen D R, Hoppe H C, Jeenah M S, de Beer F C

出版信息

J Biol Chem. 1986 Jul 25;261(21):9644-51.

PMID:3525531
Abstract

Serum amyloid A protein (apo-SAA), an acute phase reactant, is an apolipoprotein of high density lipoproteins (HDL), in particular the denser subpopulation HDL3. The structure of HDL3 isolated from humans affected by a variety of severe disease states was investigated with respect to density, size, and apolipoprotein composition, using density gradient ultracentrifugation, gradient gel electrophoresis, gel filtration, and solid phase immunoadsorption. Apo-SAA was present in HDL particles in increasing amounts as particle density increased. Apo-SAA-containing HDL3 had bigger radii than normal HDL3 of comparable density. Purified apo-SAA associated readily with normal HDL3 in vitro, giving rise to particles containing up to 80% of their apoproteins as apo-SAA. The addition of apo-SAA resulted in a displacement of apo-A-I and an increase in particle size. Acute phase HDL3 represented a mixture of particles, polydisperse with respect to apolipoprotein content; for example, some particles were isolated that contained apo-A-I, apo-A-II, and apo-SAA, whereas others contained apo-A-I and apo-SAA but no apo-A-II. We conclude that apo-SAA probably associates in the circulation of acute phase patients with existing HDL particles, causing the remodeling of the HDL shell to yield particles of bigger size and higher density that are relatively depleted of apo-A-I.

摘要

血清淀粉样蛋白A(apo-SAA)是一种急性期反应物,是高密度脂蛋白(HDL)的载脂蛋白,尤其是密度更高的亚群HDL3。采用密度梯度超速离心、梯度凝胶电泳、凝胶过滤和固相免疫吸附等方法,对从患有各种严重疾病状态的人类中分离出的HDL3的密度、大小和载脂蛋白组成进行了研究。随着颗粒密度的增加,HDL颗粒中apo-SAA的含量也在增加。含apo-SAA的HDL3的半径比密度相当的正常HDL3大。纯化的apo-SAA在体外很容易与正常HDL3结合,产生的颗粒中高达80%的载脂蛋白为apo-SAA。添加apo-SAA导致apo-A-I被取代,颗粒大小增加。急性期HDL3代表了一组颗粒的混合物,其载脂蛋白含量呈多分散性;例如,一些分离出的颗粒含有apo-A-I、apo-A-II和apo-SAA,而另一些则含有apo-A-I和apo-SAA但不含apo-A-II。我们得出结论,在急性期患者的循环中,apo-SAA可能与现有的HDL颗粒结合,导致HDL外壳重塑,产生更大尺寸和更高密度的颗粒,这些颗粒相对缺乏apo-A-I。

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J Biol Chem. 1986 Jul 25;261(21):9644-51.
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