REGULATION OF APO-B MESSENGER-RNA EXPRESSION IN LIVER AND INTESTINE DURING LIVER-REGENERATION INDUCED BY CCL4

Citation
V. Maldonado et al., REGULATION OF APO-B MESSENGER-RNA EXPRESSION IN LIVER AND INTESTINE DURING LIVER-REGENERATION INDUCED BY CCL4, Biochimica et biophysica acta, L. Lipids and lipid metabolism, 1211(1), 1994, pp. 1-6
Citations number
35
Categorie Soggetti
Biology,Biophysics
ISSN journal
00052760
Volume
1211
Issue
1
Year of publication
1994
Pages
1 - 6
Database
ISI
SICI code
0005-2760(1994)1211:1<1:ROAMEI>2.0.ZU;2-C
Abstract
Acute liver damage in CCl4-treated rats is accompanied by a decrease o f the lipoprotein particles HDL and VLDL. However, once the regenerati ve process has occurred both lipoproteins increase to values higher th an control. In this study we have further analyzed the molecular mecha nism involved in the induction of the hyperlipidemia during liver rege neration in rats treated with CCl4. The expression of apolipoprotein ( apo) B gene at the apo B mRNA editing level has been analyzed during t he regenerative process of the liver. The percent of apo B-48 and ape B-100 mRNA was determined and compared to the plasma levels of LDL and VLDL. These results confirm the existence of two different hyperlipid emic stages during liver regeneration. Total apo B mRNA is increased i n liver and intestine during both hyperlipidemic stages. The ratio of ape B-100/apo B-48 mRNA remains constant during the first hyperlipidem ic stage but the serum levels of VLDL are decreased. Then once the reg enerative 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 mR NA correlate with serum levels of VLDL that are significantly higher t han control. These results indicate that apo B gene expression is indu ced at the mRNA level in liver and intestine during liver regeneration affecting the ape B mRNA editing mechanism in a complex manner and su ggest further regulation at the translational or post-translational le vel.