Bobryshev Y V, Lord R S, Golovanova N K, Gracheva E V, Zvezdina N D, Sadovskaya V L, Prokazova N V
Surgical Professorial Unit, St Vincent's Hospital, University of New South Wales, Sydney, Australia.
Biochim Biophys Acta. 1997 Oct 24;1361(3):287-94. doi: 10.1016/s0925-4439(97)00044-6.
Immunohistochemical examination showed that sections of intimal atherosclerotic plaques contained cells and cell clusters as well as areas of extracellular matrix specifically stained with antibodies against ganglioside GM3. No immunohistochemical staining was observed in areas bordering the plaques where there was no histological evidence of atherosclerosis. To determine whether the ganglioside GM3 deposits in the intimal plaques derived directly from plasma or were synthesised by intimal cells. intimal plaque and plasma LDL were assayed for ganglioside GM3 fatty acid composition. This assay showed that more than 50% of the fatty acids of GM3 isolated from both atherosclerotic and normal intima are either minor fatty acids or those absent from LDL GM3. We conclude that the GM3 deposits present in intimal plaque arise in intimal cells and do not derive from plasma LDL.
免疫组织化学检查显示，内膜动脉粥样硬化斑块切片含有细胞和细胞簇，以及用抗神经节苷脂GM3抗体特异性染色的细胞外基质区域。在斑块边界处没有动脉粥样硬化组织学证据的区域未观察到免疫组织化学染色。为了确定内膜斑块中的神经节苷脂GM3沉积物是直接来源于血浆还是由内膜细胞合成，对内膜斑块和血浆低密度脂蛋白（LDL）进行了神经节苷脂GM3脂肪酸组成分析。该分析表明，从动脉粥样硬化内膜和正常内膜分离的GM3中，超过50%的脂肪酸要么是次要脂肪酸，要么是LDL GM3中不存在的脂肪酸。我们得出结论，内膜斑块中存在的GM3沉积物产生于内膜细胞，而非来源于血浆LDL。
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