NDLI: Lack of Socs2 expression reduces lifespan in high-growth mice

Content Provider	PubMed Central
Author	Casellas, Joaquim Medrano, Juan F.
Abstract	The high-growth (HG) phenotype in mice is characterized by a 30–50% postweaning overgrowth with a substantial increase in plasma insulin-like growth factor I (IGF1) levels, which is directly related to a deletion (hg) on chromosome 10 that includes the suppressor of cytokine signaling 2 (Socs2) gene. Reduced plasma IGF1 levels have been associated with extended lifespan in mice, although the aging-related effects of abnormally high IGF1 levels without elevated growth hormone levels have never been assessed in mammals. Within this context, the hg deletion was introgressed into C57BL/6J (B6) and FVB backgrounds, and a survival analysis was performed on the longevity records of 200 B6 (91 wild-type and 109 homozygous hg mutants) and 69 FVB (32 wild-type and 37 hg mutants) mice. Longevity was examined using a piecewise Weibull proportional hazards model solved through a Bayesian perspective and Markov chain Monte Carlo sampling. Lifespan was significantly reduced in both strains in homozygous hg mice, with a death risk between 3.689 (B6) and 4.347 (FVB) times higher than in wild-type mice (non-overlapped highest posterior density regions at 95%). These results highlight the effects of the Socs2 gene on aging regulation, likely related with variations described in plasma IGF1 levels. This result is consistent with previous research in dwarf mutant mice and other species, and characterizes the HG mutant mice as a unique and interesting animal model for accelerated aging research.
Related Links	http://dx.doi.org/10.1007/s11357-008-9064-1
Ending Page	249
Page Count	5
Starting Page	245
File Format	PDF
ISSN	01619152
e-ISSN	15744647
Journal	Age
Issue Number	4
Volume Number	30
Language	English
Publisher	Springer Netherlands
Publisher Date	2008-12-01
Access Restriction	Open
Rights Holder	Springer Netherlands
Subject Keyword	Ageing Geriatrics and Gerontology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Aging Geriatrics and Gerontology

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