Distribution of endogenous apoprotein B-containing lipoproteins in normal and injured aortas of normocholesterolemic rabbits.
Distribution of endogenous apoprotein B-containing lipoproteins in normal and injured aortas of normocholesterolemic rabbits.
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正常胆固醇血症兔正常和损伤主动脉中内源性含脱辅基蛋白 B 的脂蛋白分布。
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发表时间：
1992
期刊：
影响因子：
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通讯作者：
S. Moore
中科院分区：
文献类型：
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作者：
Z. Galis;L. Ghitescu;Z. Li;M. Alavi;S. Moore
本文研究了内源性载脂蛋白B(Apo B)在正常和球囊导管损伤的标准喂养兔主动脉中的分布。用免疫细胞化学方法，用兔载脂蛋白B抗体，用光镜和电子显微镜观察了载脂蛋白B在整个主动脉壁和单个组织室内的分布。载脂蛋白B穿过管壁的浓度从管腔前沿向正常主动脉中层急剧下降。强烈的表面反应主要是由于内皮细胞的大量但特异的标记。在细胞外空间的最内侧区域也检测到显著浓度的载脂蛋白B。与内膜层标记相关的特征表明内皮细胞对载脂蛋白B有强烈的摄取和跨细胞运输。与之形成鲜明对比的是，正常的平滑肌细胞似乎没有被标记。在先前损伤的主动脉中，在再生内皮细胞覆盖的区域存在相同的表面载脂蛋白B强标记特征，而在那些持续脱内皮化的血管中则不存在。这些区域的平滑肌细胞对载脂蛋白B的摄取较低。损伤的主动脉深层间质区载脂蛋白B浓度升高，提示细胞外基质对载脂蛋白B的积聚有贡献。这在晚期病变中尤其明显，选择性地发生在新生内皮覆盖的新生内膜内。相当均匀的标记模式伴随着小的脂质颗粒沉积，表明循环脂蛋白直接在细胞外积累。细胞坏死区内可见强标记的泡沫细胞和不规则分布的载脂蛋白B。细胞和细胞外成分的损伤反应可在正常胆固醇血症动物的主动脉内触发脂蛋白积聚，其特征是动脉粥样硬化。
The distribution of endogenous apolipoprotein B (apo B) was studied in both normal and balloon catheter-injured aortas of standard fed rabbits. Using light and electron microscopy, the distribution within entire aortic walls and individual tissue compartments was investigated by immunocytochemistry using an antibody raised against rabbit apo B. The concentration of apo B across the vessel wall dropped sharply from the luminal front towards the media of the normal aortas. The strong superficial reaction was mainly due to a heavy, yet specific, labelling of endothelial cells. Significant concentrations of apo B were also detected within the innermost regions of the extracellular space. The characteristics associated with the labelling of the intimal layer suggested an intense uptake and transcellular transport of apo B by endothelial cells. In contradistinction, normal smooth muscle cells did not appear to be labelled. In the previously injured aortas, the same features of strong superficial apo B labelling were present in the areas covered by regenerated endothelial cells, but not in those persistently deendothelialized. The smooth muscle cells of these regions appeared to show a low uptake of apo B. The increased concentrations of apo B in deeper interstitial areas of injured aortas, indicated the contribution of the extracellular matrix to apo B accumulation. This was especially prominent in the advanced lesions, selectively developed within neointima covered by regenerated endothelium. A rather uniform labelling pattern accompanying small lipid particle deposits, suggested a direct extracellular accumulation of circulating lipoproteins. Intensely labelled foam cells and irregularly distributed apo B within areas of cellular necrosis were detected as well. Injury-mediated responses of the cellular and extracellular aortic components can trigger the development of lipoprotein accumulations characteristic of atherosclerosis within aortas of normocholesterolemic animals.