Senescent accelerated mouse (SAM): A model that binds in vivo and in vitro aging

Y. E. Yegorov, I. V. Semenova, D. N. Karachentsev, M. L. Semenova, S. S. Akimov, I. N. Yegorova, A. V. Zelenin

Research output: Contribution to journalArticlepeer-review

Abstract

It is known that the longevity of senescence accelerated mouse (SAM) is significantly reduced. We intended to check the relationship of the SAM shortened longevity with some characteristics of their cells in culture. Investigations of lifespans of SAM embryo fibroblasts, survival of senescent nondividing cells, endogenous β-galactosidase activity, telomerase activity, and telomere length were conducted. There is correlation of longevity of SAMP1 (senescence prone strain), SAMR1 (accelerated senescence resistant strain), and CBA mice with proliferative lifespans of their embryo fibroblasts in vitro as well as with the survival time of nondividing senesced embryo fibroblasts. The premature senescence of SAMP1 and SAMR1 fibroblasts is associated with accelerated accumulation of the β-galactosidase-positive cells. Terminal restriction fragments of chromosomes of SAMP1 are more heterogeneous than SAMR1 ones. There is relatively high telomerase activity (in comparison with CBA mice) in SAM embryos and cell cultures. This activity rapidly decreases during growth in vitro and is restored after spontaneous transformation occurring at a high frequency in both strains. SAM is a very promising model for studying the relationships of body aging and cell senescence in culture.

Original languageEnglish (US)
Pages (from-to)39-47
Number of pages9
JournalJournal of Anti-Aging Medicine
Volume4
Issue number1
DOIs
StatePublished - Jan 1 2001
Externally publishedYes

ASJC Scopus subject areas

  • Aging

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