Dashti N, Smith E A, Alaupovic P
Lipoprotein and Atherosclerosis Research Program, Oklahoma Medical Research Foundation, Oklahoma City 73104.
J Lipid Res. 1990 Jan;31(1):113-23.
The production of lipids, apolipoproteins (apo), and lipoproteins induced by oleic acid has been examined in Caco-2 cells. The rates of accumulation in the control medium of 15-day-old Caco-2 cells of triglycerides, unesterified cholesterol, and cholesteryl esters were 102 +/- 8, 73 +/- 5, and 11 +/- 1 ng/mg cell protein/h, respectively; the accumulation rates for apolipoproteins A-I, B, C-III, and E were 111 +/- 9, 53 +/- 4, 13 +/- 1, and 63 +/- 4 ng/mg cell protein/h, respectively. Whereas apolipoproteins A-IV and C-II were detected by immunoblotting, apoA-II was absent in most culture media. In contrast to an early production of apolipoproteins A-I and E occurring 2 days after plating, the apoB expression appeared to be differentiation-dependent and was not measurable in the medium until the sixth day post-confluency. In the control medium, very low density lipoproteins (VLDL), low density lipoproteins (LDL), high density lipoproteins (HDL), and lipid-poor very high density lipoproteins (VHDL) accounted for 12%, 46%, 18%, and 24% of the total lipid and apolipoprotein contents, respectively. The triglyceride-rich VLDL contained mainly apoE (75%) and apoB (23%), while the protein moiety of LDL was composed of apoB (59%), apoE (20%), apoA-I (15%), and apoC-III (6%). The cholesterol-rich HDL contained mainly apoA-I (69%) and apoE (27%). In the control medium, major portions of apolipoproteins B and C-III (93-97%) were present in LDL, whereas the main parts of apoA-I (92%) and apoE (76%) were associated with HDL and VHDL. Oleate increased the production of triglycerides 10-fold, cholesteryl esters 7-fold, and apoB 2- to 4-fold. There was also a moderate increase (39%) in the production of apoC-III but no significant changes in those of apolipoproteins A-I and E. These increases were reflected mainly in a 55-fold elevation in the concentration of VLDL, and a 2-fold increase in the level of LDL; there were no significant changes in HDL and VHDL. VLDL contained the major parts of total neutral lipids (74-86%), apoB (65%), apoC-III (81%) and apoE (58%). In the presence of oleate, the VLDL, LDL, HDL, and VHDL accounted for 76%, 15%, 3%, and 6% of the total lipoproteins, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)
已在Caco-2细胞中研究了油酸诱导的脂质、载脂蛋白（apo）和脂蛋白的产生。15日龄Caco-2细胞在对照培养基中甘油三酯、未酯化胆固醇和胆固醇酯的积累速率分别为102±8、73±5和11±1 ng/mg细胞蛋白/小时；载脂蛋白A-I、B、C-III和E的积累速率分别为111±9、53±4、13±1和63±4 ng/mg细胞蛋白/小时。虽然通过免疫印迹检测到了载脂蛋白A-IV和C-II，但大多数培养基中不存在apoA-II。与接种后2天出现的载脂蛋白A-I和E的早期产生相反，apoB的表达似乎依赖于分化，直到汇合后第六天才在培养基中检测到。在对照培养基中，极低密度脂蛋白（VLDL）、低密度脂蛋白（LDL）、高密度脂蛋白（HDL）和低脂极高密度脂蛋白（VHDL）分别占总脂质和载脂蛋白含量的12%、46%、18%和24%。富含甘油三酯的VLDL主要含有apoE（75%）和apoB（23%），而LDL的蛋白质部分由apoB（59%）、apoE（20%）、apoA-I（15%）和apoC-III（6%）组成。富含胆固醇的HDL主要含有apoA-I（69%）和apoE（27%）。在对照培养基中，载脂蛋白B和C-III的大部分（93 - 97%）存在于LDL中，而apoA-I（92%）和apoE（76%）的主要部分与HDL和VHDL相关。油酸使甘油三酯的产生增加了10倍，胆固醇酯增加了7倍，apoB增加了2至4倍。apoC-III的产生也有适度增加（39%），但载脂蛋白A-I和E的产生没有显著变化。这些增加主要反映在VLDL浓度升高55倍，LDL水平升高2倍；HDL和VHDL没有显著变化。VLDL包含总中性脂质的主要部分（74 - 86%）、apoB（65%）、apoC-III（81%）和apoE（58%）。在油酸存在的情况下，VLDL、LDL、HDL和VHDL分别占总脂蛋白的76%、15%、3%和6%。（摘要截断于400字）
