Wild type ApoA-II gene does not rescue senescence-accelerated mouse (SAMP1) from short life span and accelerated mortality

J. Wang, T. Matsushita, K. Kogishi, C. Xia, A. Ohta, T. Chiba, A. Nakamura, H. Kondo, M. Mori, M. Hosokawa, K. Higuchi*

*この研究の対応する著者

研究成果: Article査読

5 被引用数 (Scopus)

抄録

Biochemical and genetic data suggest that the Apoa2c allele of the apolipoprotein A-II gene causes severe senile amyloidosis (AApoAII) in SAMP1, a mouse model for accelerated senescence. We analyzed the effects of replacement ofApoa2c in SAMP1 mice with non-amyloidogenic Apoa2b on amyloidosis, lipoprotein metabolism, and progression of senescence using a congenic strain, P1.R1-Apoa2b, which has the Apoa2b chromosome region of SAMR1 in the genome of SAMP1. Age-associated amyloid deposition was not observed, but plasma concentrations of apoA-II protein and HDL-cholesterol decreased with age in P1.R1-Apoa2b. P1.R1-Apoa2b showed lower scores of senescence than did SAMP1. However, the life span and mortality rate doubling time were similar in P1.R1-Apoa2b and SAMP1. These results suggest that replacement of Apoa2c with non-amyloidogenic Apoa2b does not rescue SAMP1 mice from a short life span and accelerated mortality.

本文言語English
ページ(範囲)B432-B439
ジャーナルJournals of Gerontology - Series A Biological Sciences and Medical Sciences
55
9
DOI
出版ステータスPublished - 2000
外部発表はい

ASJC Scopus subject areas

  • 加齢科学
  • 老年医学

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