P66SHC deletion improves fertility and progeric phenotype of late‐generation TERC‐deficient mice but not their short lifespan

P66SHC deletion improves fertility and progeric phenotype of late‐generation TERC‐deficient mice but not their short lifespan

Oxidative stress and telomere attrition are considered the driving factors of aging. As oxidative damage to telomeric DNA favors the erosion of chromosome ends and, in turn, telomere shortening increases the sensitivity to pro‐oxidants, these two factors may trigger a detrimental vicious cycle. To c...

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Main Authors: Giorgio, Marco, Stendardo, Massimo, Migliaccio, Enrica, Pelicci, Pier Giuseppe
Format: Online
Language:English
Published: John Wiley and Sons Inc. 2016
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4854904/
id pubmed-4854904
recordtype oai_dc
spelling pubmed-48549042016-06-16 P66SHC deletion improves fertility and progeric phenotype of late‐generation TERC‐deficient mice but not their short lifespan Giorgio, Marco Stendardo, Massimo Migliaccio, Enrica Pelicci, Pier Giuseppe Original Articles Oxidative stress and telomere attrition are considered the driving factors of aging. As oxidative damage to telomeric DNA favors the erosion of chromosome ends and, in turn, telomere shortening increases the sensitivity to pro‐oxidants, these two factors may trigger a detrimental vicious cycle. To check whether limiting oxidative stress slows down telomere shortening and related progeria, we have investigated the effect of p66SHC deletion, which has been shown to reduce oxidative stress and mitochondrial apoptosis, on late‐generation TERC (telomerase RNA component)‐deficient mice having short telomeres and reduced lifespan. Double mutant (TERC −/− p66SHC −/−) mice were generated, and their telomere length, fertility, and lifespan investigated in different generations. Results revealed that p66SHC deletion partially rescues sterility and weight loss, as well as organ atrophy, of TERC‐deficient mice, but not their short lifespan and telomere erosion. John Wiley and Sons Inc. 2016-03-10 2016-06 /pmc/articles/PMC4854904/ /pubmed/26968134 http://dx.doi.org/10.1111/acel.12448 Text en © 2016 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Giorgio, Marco
Stendardo, Massimo
Migliaccio, Enrica
Pelicci, Pier Giuseppe
spellingShingle Giorgio, Marco
Stendardo, Massimo
Migliaccio, Enrica
Pelicci, Pier Giuseppe
P66SHC deletion improves fertility and progeric phenotype of late‐generation TERC‐deficient mice but not their short lifespan
author_facet Giorgio, Marco
Stendardo, Massimo
Migliaccio, Enrica
Pelicci, Pier Giuseppe
author_sort Giorgio, Marco
title P66SHC deletion improves fertility and progeric phenotype of late‐generation TERC‐deficient mice but not their short lifespan
title_short P66SHC deletion improves fertility and progeric phenotype of late‐generation TERC‐deficient mice but not their short lifespan
title_full P66SHC deletion improves fertility and progeric phenotype of late‐generation TERC‐deficient mice but not their short lifespan
title_fullStr P66SHC deletion improves fertility and progeric phenotype of late‐generation TERC‐deficient mice but not their short lifespan
title_full_unstemmed P66SHC deletion improves fertility and progeric phenotype of late‐generation TERC‐deficient mice but not their short lifespan
title_sort p66shc deletion improves fertility and progeric phenotype of late‐generation terc‐deficient mice but not their short lifespan
description Oxidative stress and telomere attrition are considered the driving factors of aging. As oxidative damage to telomeric DNA favors the erosion of chromosome ends and, in turn, telomere shortening increases the sensitivity to pro‐oxidants, these two factors may trigger a detrimental vicious cycle. To check whether limiting oxidative stress slows down telomere shortening and related progeria, we have investigated the effect of p66SHC deletion, which has been shown to reduce oxidative stress and mitochondrial apoptosis, on late‐generation TERC (telomerase RNA component)‐deficient mice having short telomeres and reduced lifespan. Double mutant (TERC −/− p66SHC −/−) mice were generated, and their telomere length, fertility, and lifespan investigated in different generations. Results revealed that p66SHC deletion partially rescues sterility and weight loss, as well as organ atrophy, of TERC‐deficient mice, but not their short lifespan and telomere erosion.
publisher John Wiley and Sons Inc.
publishDate 2016
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4854904/
_version_ 1613574712502255616

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