REGULATION OF CHOLESTEROL IN VASCULAR ENDOTHELIUM

脂蛋白的调节作用及其机制 MVA代谢及其作为培养细胞活性因子的作用 将用正常二倍体细胞(毛细血管)作为模型进行分析 内皮细胞(CE)、血管平滑肌细胞)和AN 已建立的细胞系(MDCK细胞)。能力很低 密度脂蛋白(VLDL)是低密度脂蛋白的前体 细胞的形状和增殖将通过培养来确定 暴露于或不暴露于紧凑型。他们的影响将与 高密度脂蛋白。作为一种特异的极低密度脂蛋白和高密度脂蛋白代谢反应， 将测量它们对HMG-CoA还原酶的影响，并 被认为是底物流入甾醇的反映 非固醇代谢物。我们将确定哪种关键的非甾醇 MVA代谢产生的产物将与 控制细胞增殖和细胞形状，这将解释 脂蛋白作为能力因子的能力。我们的 注意力将集中在萜类化合物的合成上，这些化合物 翻译后修饰特定多肽。的影响 高密度脂蛋白、极低密度脂蛋白和分离的成分(磷脂脂质体， 载脂蛋白)对萜烯合成的影响及其掺入 多肽及b-成纤维细胞生长因子的作用 对于CE单元)，将使用AS模型来检查这种过程 稀疏的CE细胞暴露或不暴露于致密素。

The effect and mechanisms through which lipoproteins regulate MVA metabolism and act as competence factors for cultured cells will be analyzed using as models normal diploid cells (capillary endothelial cells (CE), vascular smooth muscle cells) and an established cell line (MDCK cells). The ability of very low density lipoproteins (VLDL) which are LDL precursors to support cell shape and proliferation will be determined using cultures exposed or not to compactin. Their effects will be compared to that of HDL. As a specific VLDL and HDL metabolic response, their effect on HMG-CoA reductase will be measured and considered as a reflection of substrate flux into sterols and nonsterol metabolites. We will determine which key nonsterol products resulting from MVA metabolism would be relevant to the control of cell proliferation and cell shape and would explain the ability of lipoproteins to act as competence factors. Our attention will be focused on the synthesis of terpenes which modify specific polypeptides post translationally. The effect of HDL, VLDL and isolated components (phospholipid liposomes, apolipoproteins) on terpene synthesis and their incorporation into polypeptides as well as the effect of b FGF ( a progression factor for CE cells) on such a process will be examined using as models sparse CE cells exposed or not to compactin.