Maldonado V, Chan L, Meléndez J, Rincón A R, Zhu H J, Panduro A
Department of Gastroenterology, Instituto Nacional de la Nutrición, Tlalpan, México D.F.
Biochim Biophys Acta. 1994 Feb 10;1211(1):1-6. doi: 10.1016/0005-2760(94)90131-7.
Acute liver damage in CCl4-treated rats is accompanied by a decrease of the lipoprotein particles HDL and VLDL. However, once the regenerative process has occurred both lipoproteins increase to values higher than control. In this study we have further analyzed the molecular mechanism involved in the induction of the hyperlipidemia during liver regeneration in rats treated with CCl4. The expression of apolipoprotein (apo) B gene at the apo B mRNA editing level has been analyzed during the regenerative process of the liver. The percent of apo B-48 and apo B-100 mRNA was determined and compared to the plasma levels of LDL and VLDL. These results confirm the existence of two different hyperlipidemic stages during liver regeneration. Total apo B mRNA is increased in liver and intestine during both hyperlipidemic stages. The ratio of apo B-100/apo B-48 mRNA remains constant during the first hyperlipidemic stage but the serum levels of VLDL are decreased. Then once the regenerative process has occurred, the steady-state levels of total apo B mRNA remaining, increased with higher amounts of apo B-100 than apo B-48. At this experimental time point the high levels of total apo B mRNA correlate with serum levels of VLDL that are significantly higher than control. These results indicate that apo B gene expression is induced at the mRNA level in liver and intestine during liver regeneration affecting the apo B mRNA editing mechanism in a complex manner and suggest further regulation at the translational or post-translational level.
四氯化碳处理的大鼠急性肝损伤伴随着脂蛋白颗粒高密度脂蛋白(HDL)和极低密度脂蛋白(VLDL)的减少。然而,一旦再生过程发生,这两种脂蛋白都会增加到高于对照的值。在本研究中,我们进一步分析了四氯化碳处理的大鼠肝再生过程中高脂血症诱导所涉及的分子机制。在肝脏再生过程中,分析了载脂蛋白(apo)B基因在apo B mRNA编辑水平的表达。测定了apo B-48和apo B-100 mRNA的百分比,并与低密度脂蛋白(LDL)和极低密度脂蛋白(VLDL)的血浆水平进行比较。这些结果证实了肝再生过程中存在两个不同的高脂血症阶段。在两个高脂血症阶段,肝脏和肠道中的总apo B mRNA均增加。在第一个高脂血症阶段,apo B-100/apo B-48 mRNA的比值保持恒定,但极低密度脂蛋白(VLDL)的血清水平降低。然后,一旦再生过程发生,剩余的总apo B mRNA的稳态水平增加,其中apo B-100的量高于apo B-48。在这个实验时间点,总apo B mRNA的高水平与显著高于对照的极低密度脂蛋白(VLDL)血清水平相关。这些结果表明,肝再生过程中肝脏和肠道中apo B基因在mRNA水平被诱导,以复杂的方式影响apo B mRNA编辑机制,并提示在翻译或翻译后水平存在进一步调控。