Involvement of a cellular surface factor(s) in lipid-free apolipoprotein-mediated cellular cholesterol efflux

Involvement of a cellular surface factor(s) in lipid-free apolipoprotein-mediated cellular cholesterol efflux
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DOI:
10.1016/0005-2760(95)00165-4
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发表时间:
1995-12-07
期刊:
BIOCHIMICA ET BIOPHYSICA ACTA-LIPIDS AND LIPID METABOLISM
影响因子:
--
通讯作者:
Yokoyama, S
Yokoyama, S
中科院分区:
其他
文献类型:
--
作者:
Li, QQ;Czarnecka, H;Yokoyama, S

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研究了无脂载脂蛋白介导的细胞脂质外排中细胞表面因子的参与。无脂人载脂蛋白(apo) A-I从小鼠腹膜巨噬细胞和大鼠主动脉平滑肌细胞中产生胆固醇和磷脂的净流出。与我们之前的观察结果一致(Li, Q., Komaba, A. and Yokoyama, S. (1993) Biochemistry 32,4597 -4603),通过这种机制从平滑肌细胞释放的脂质中胆固醇与磷脂的比例要比巨噬细胞低得多。另一方面,游离apoa - 1不会引起人红细胞的脂质外排。相反,在这三种细胞膜上都观察到细胞胆固醇向HDL的明显外排。胰蛋白酶处理培养的巨噬细胞完全抑制apoa - i介导的胆固醇和磷脂外排。平滑肌细胞也表现出胰蛋白酶完全抑制apoa - i介导的细胞脂质外排,只是需要更长时间的酶孵育。用胰蛋白酶进行同样的细胞处理,即使经过长时间的孵育,对细胞内胆固醇向高密度脂蛋白和无载脂蛋白脂质微乳的明显外排也只有有限的影响。因此,游离载脂蛋白介导的细胞脂质外排似乎依赖于红细胞可能缺乏的胰蛋白酶敏感细胞表面因子,这与细胞和脂蛋白之间的物理化学胆固醇交换反应不同。
Involvement of cellular surface factors in cellular lipid efflux mediated by lipid-free apolipoprotein has been investigated. Lipid-free human apolipoprotein (apo) A-I generated net efflux of cholesterol and phospholipid from mouse peritoneal macrophages and rat aorta smooth muscle cells. Ratio of cholesterol to phospholipid was much lower in the lipid released by this mechanism from the smooth muscle cells than that from the macrophages, in agreement with our previous observation (Li, Q., Komaba, A. and Yokoyama, S. (1993) Biochemistry 32, 4597-4603). On the other hand, free apoA-I did not cause any lipid efflux from human erythrocytes, In contrast, apparent efflux of cellular cholesterol to HDL was similarly observed from all of these three cellular membranes. Trypsin treatment of the cultured macrophages completely inhibited apoA-I-mediated efflux of cholesterol and phospholipid. Smooth muscle cells also showed complete inhibition of the apoA-I-mediated cellular lipid efflux by trypsin treatment except that it required longer incubation with the enzyme. The same cellular treatment with trypsin even by prolonged incubation had only a limited effect on apparent cellular cholesterol efflux to HDL and apolipoprotein-free lipid microemulsions. Thus, free apolipoprotein-mediated cellular lipid efflux seems to depend on a trypsin-susceptible cellular surface factor(s) that erythrocytes may lack, being distinct from physicochemical cholesterol exchange reaction between cell and lipoprotein.