title: Regulation of apo B mRNA expression in liver and intestine during liver regeneration induced by CCl4.
abstract: 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.
authors.affiliation: Department of Gastroenterology, Instituto Nacional de la Nutrición, Tlalpan, México D.F.
authors.forename: V
authors.initials: V
authors.lastname: Maldonado
authors.forename: L
authors.initials: L
authors.lastname: Chan
authors.forename: J
authors.initials: J
authors.lastname: Meléndez
authors.forename: A R
authors.initials: AR
authors.lastname: Rincón
authors.forename: H J
authors.initials: HJ
authors.lastname: Zhu
authors.forename: A
authors.initials: A
authors.lastname: Panduro
mesh_terms: D000818:Animals; D001055:Apolipoproteins B / Q000235:genetics*; D001483:Base Sequence; D002251:Carbon Tetrachloride; D005786:Gene Expression Regulation / Q000187:drug effects; D006949:Hyperlipidemias / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000187:drug effects*; D008075:Lipoproteins, HDL / Q000097:blood; D008079:Lipoproteins, VLDL / Q000097:blood; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008115:Liver Regeneration; D008297:Male; D008969:Molecular Sequence Data; D012333:RNA, Messenger / Q000032:analysis*; D051381:Rats; D017208:Rats, Wistar
chemical_list: D001055:Apolipoproteins B; D008075:Lipoproteins, HDL; D008079:Lipoproteins, VLDL; D012333:RNA, Messenger; D002251:Carbon Tetrachloride