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Journal of Lipid Research, Vol 33, 1753-1764, Copyright © 1992 by Lipid Research, Inc.
K Higuchi, K Kitagawa, K Kogishi and T Takeda
Apolipoprotein B (apoB) mRNA is modified by a post-transcriptional editing
reaction (C to U) changing a glutamine (CAA) to a translational stop codon
(UAA) and producing apoB-48 mRNA in mammalian liver and intestine.
Developmental and age-related changes in apoB mRNA editing were studied
using two mouse strains with different aging processes (SAM-R/1 with a
normal aging process and SAM-P/1 with an accelerated aging process). During
growth of both strains, the proportion of unedited (apoB-100) mRNA
decreased from 80% in the fetal liver at the 17th day of gestation to 30%
in the liver of mature 2-month-old mice. Age-associated increase in the
proportion of hepatic apoB-100 mRNA was observed from the age of 18 months
in the SAM-R/1 strain. In the SAM- P/1 strain, apoB-100 mRNA in the liver
continued to increase from the age of 10 months to death. The profiles of
developmental and age- related changes in the proportion of two serum apoB
isoproteins (apoB- 100 and apoB-48) followed the extent of hepatic apoB
mRNA editing. Age- related changes in the extent of apoB mRNA editing in
the small intestine were not observed in either strain. A slight expression
of apoB was detected by reverse transcriptase-polymerase chain reaction in
the kidney, stomach, and colon, and age-associated change in the extent of
editing was observed in the kidney. These correlated changes in apoB mRNA
editing and serum apoB proteins suggest that RNA editing may be one
mechanism involved in the regulation of lipoprotein biogenesis in
biological development and in senescent mice. An age-associated decrease in
the extent of hepatic apoB mRNA editing and increases of the proportion of
serum apoB-100 protein were observed in senescent mice.
ARTICLES
Developmental and age-related changes in apolipoprotein B mRNA editing in mice
Department of Senescence Biology, Kyoto University, Japan.
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