INCORPORATION OF 14C-LABELED ACETATE INTO LIPID BY ISOLATED FOAM CELLS AND BY ATHEROSCLEROTIC ARTERIAL INTIMA
INCORPORATION OF 14C-LABELED ACETATE INTO LIPID BY ISOLATED FOAM CELLS AND BY ATHEROSCLEROTIC ARTERIAL INTIMA
复制标题
DOI：
10.1161/01.res.21.5.593
复制
发表时间：
1967-01-01
影响因子：
20.1
通讯作者：
WILKINSON, GK
中科院分区：
文献类型：
--
作者：
DAY, AJ;WILKINSON, GK
本文研究了体外培养的兔动脉粥样硬化内膜合成脂质的能力，并与从内膜损伤处分离的泡沫细胞进行了比较。在动脉粥样硬化的动脉内膜中，14 C-标记的乙酸盐容易掺入脂质部分中，大部分标记物存在于磷脂和胆固醇酯脂肪酸部分中。甘油三酯、脂肪酸和胆固醇的掺入量极低。合成的主要磷脂是卵磷脂，但也发生了磷脂酰肌醇、磷脂酰乙醇胺和鞘磷脂的显著掺入。合成的脂肪酸主要在磷脂部分中饱和。胆固醇酯脂肪酸中存在较多的单不饱和脂肪酸，但在两个部分中，乙酸酯标记的多不饱和脂肪酸很少。孤立的泡沫细胞也被证明将14 C-标记的乙酸酯磷脂和胆固醇酯脂肪酸。然而，泡沫细胞，纳入一个显着较高比例的乙酸酯胆固醇酯比整个内膜。由泡沫细胞合成的脂肪酸在磷脂和胆固醇酯组分中比在整个内膜中更多不饱和。这些发现的相关性的起源脂质在动脉粥样硬化病变进行了讨论。
The synthesis of lipid by rabbit atherosclerotic intima incubated in vitro has been investigated and compared with that of foam cells isolated from intimal lesions. In the atherosclerotic arterial intima, 14c -labeled acetate is readily incorporated into the lipid fraction, most of the label being found in the phospholipid and cholesterol ester fatty acid fractions. Minimal incorporation into triglyceride, fatty acid, and cholesterol occurred. The major phospholipid synthesized was lecithin but significant incorporation into phosphatidyl inositol, phosphatidyl ethanolamine, and sphingomyelin also took place. The fatty acids synthesized were predominantly saturated in the phospholipid fraction. More monoun-saturated fatty acids were present in the cholesterol ester fatty acids, but in both moieties little polyunsaturated fatty acids were labeled by the acetate. Isolated foam cells were also shown to incorporate 14c-labeled acetate into both phospholipid and cholesterol ester fatty acids. The foam cells, however, incorporated a significantly higher proportion of acetate into cholesterol ester than did the whole intima. The fatty acids synthesized by the foam cells were more polyunsaturated in both the phospholipid and the cholesterol ester fraction than was the case with the whole intima. The relevance of these findings to the origin of lipid in the atherosclerotic lesion is discussed.