Uptake of high-density lipoprotein-associated apoprotein A-I and cholesterol esters by 16 tissues of the rat in vivo and by adrenal cells and hepatocytes in vitro.
Uptake of high-density lipoprotein-associated apoprotein A-I and cholesterol esters by 16 tissues of the rat in vivo and by adrenal cells and hepatocytes in vitro.
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DOI：
10.1016/s0021-9258(20)71160-9
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发表时间：
1985-01
期刊：
影响因子：
--
通讯作者：
Christopher;Ray C. Pittman;Morton Civen;Daniel Steinberg
中科院分区：
文献类型：
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作者：
Christopher;Ray C. Pittman;Morton Civen;Daniel Steinberg
用非降解示踪剂（共价连接的125 I-酪胺-纤维二糖示踪apo-A-I和[3 H]胆固醇亚油基醚示踪胆固醇酯）双标记大鼠HDL，在大鼠16种组织中估计高密度脂蛋白（HDL）相关载脂蛋白A-I和胆固醇酯的摄取。这两种标记物仍然与血浆中的HDL组分相关，充分追踪其未标记的对应物，并在其摄取部位被很好地捕获。肾上腺、卵巢和肝脏对胆固醇醚的摄取率分别比apo-A-I高7倍、4倍和2倍。胆固醇醚和apo-A-I在其他组织（肾脏除外）中的摄取率大致相等。在大鼠肾上腺细胞和肝细胞的原代培养物中也观察到HDL胆固醇醚相对于HDL apo-A-I的不成比例摄取。两种细胞类型中两种基团的摄取均显示饱和性。肾上腺细胞摄取[3 H]胆固醇醚的绝对速率和醚摄取与apo-A-I摄取的比值均大于肝细胞，与体内观察结果一致。使用[3 H]胆固醇酯生物标记的HDL获得了非常相似的结果。[3 H]胆固醇醚的不成比例摄取并没有显著降低从HDL的apo-E消耗，也没有通过apo-E的还原甲基化来阻断其受体的识别。然而，apo-A-I的吸收减少，这表明apo-E介导含有apo-A-I的颗粒的吸收，但不会导致[3 H]胆固醇醚的不成比例的吸收。
The uptake of high-density lipoprotein (HDL)-associated apolipoprotein A-I and cholesterol esters was estimated in 16 tissues of the rat using rat HDL doubly labeled with nondegradable tracers; covalently attached 125I-tyramine-cellobiose traced apo-A-I, and [3H]cholesteryl linoleyl ether traced cholesterol esters. Both labels remained associated with the HDL fraction in the plasma, adequately traced their unlabeled counterparts, and were well trapped at their sites of uptake. Cholesteryl ether was taken up at a greater fractional rate than apo-A-I by adrenal, ovary, and liver: 7-fold, 4-fold, and 2-fold greater, respectively. The rates of uptake of cholesteryl ether and apo-A-I were about equal in the other tissues (except kidney). The disproportionate uptake of HDL cholesteryl ether relative to HDL apo-A-I was also observed in primary cultures of rat adrenal cells and hepatocytes. Uptake of both moieties in both cell types showed saturability. Both the absolute rate of uptake of [3H]cholesteryl ether and the ratio of ether uptake to apo-A-I uptake were greater in adrenal cells than in hepatocytes, consonant with the in vivo observations. Very similar results were obtained using HDL biologically labeled with [3H]cholesterol esters. The disproportionate uptake of [3H]cholesteryl ether was not significantly decreased by depletion of apo-E from the HDL nor by reductive methylation of the apo-E to block its recognition by receptors. However, apo-A-I uptake was decreased, suggesting that apo-E mediates the uptake of particles containing apo-A-I but does not contribute to the disproportionate uptake of [3H]cholesteryl ether.