Interleukin 6 knock-out Inhibits aging-related Accumulation of p53 in the Mouse Myocardium

Interleukin 6 knock-out Inhibits aging-related Accumulation of p53 in the Mouse Myocardium Abstract Interleukin 6 (IL6) and p53 are linked by mutual regulatory mechanisms and are both upregulated in aging. The aim of this study was to evaluate the effects of aging and IL-6 on expression of p53 in the mouse heart. Male C57BL6/J wild-type (WT) and IL6 knock-out (IL6KO) mice at the age of 4-5 months (young adult) and 24-30 months (old) were used. Myocardial expression of proteins: p53, p21, Mdm2, and phospho-Akt/Akt was estimated using western blotting and expression of p53 and p21 mRNA using real-time-PCR. Expression of p53 protein was lower in IL6KO than in WT hearts. Aging caused significant upregulation of p53 protein level, however it was significantly higher in old WT than in old IL6KO hearts (p<0.05). Similar p53 mRNA levels in all groups implied IL6 influence on age-related proteasomal degradation of p53. Localization of p53 mainly in the extranuclear compartment and lack of p21 upregulation in aged hearts may suggest quenched transcriptional activity of p53 despite increased abundance of p53. We conclude that lack of IL6 attenuates expression of p53 protein in the hearts of young mice and diminishes its accumulation with aging by post-transcriptional mechanisms, however this is not related to altered phenotype of aging heart. p53, Mdm-2, interleukin 6, heart, aging, mouse © The Author(s) 2018. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journals of Gerontology Series A: Biomedical Sciences and Medical Sciences Oxford University Press

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Publisher
Oxford University Press
Copyright
© The Author(s) 2018. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
ISSN
1079-5006
eISSN
1758-535X
D.O.I.
10.1093/gerona/gly105
Publisher site
See Article on Publisher Site

Abstract

Abstract Interleukin 6 (IL6) and p53 are linked by mutual regulatory mechanisms and are both upregulated in aging. The aim of this study was to evaluate the effects of aging and IL-6 on expression of p53 in the mouse heart. Male C57BL6/J wild-type (WT) and IL6 knock-out (IL6KO) mice at the age of 4-5 months (young adult) and 24-30 months (old) were used. Myocardial expression of proteins: p53, p21, Mdm2, and phospho-Akt/Akt was estimated using western blotting and expression of p53 and p21 mRNA using real-time-PCR. Expression of p53 protein was lower in IL6KO than in WT hearts. Aging caused significant upregulation of p53 protein level, however it was significantly higher in old WT than in old IL6KO hearts (p<0.05). Similar p53 mRNA levels in all groups implied IL6 influence on age-related proteasomal degradation of p53. Localization of p53 mainly in the extranuclear compartment and lack of p21 upregulation in aged hearts may suggest quenched transcriptional activity of p53 despite increased abundance of p53. We conclude that lack of IL6 attenuates expression of p53 protein in the hearts of young mice and diminishes its accumulation with aging by post-transcriptional mechanisms, however this is not related to altered phenotype of aging heart. p53, Mdm-2, interleukin 6, heart, aging, mouse © The Author(s) 2018. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices)

Journal

The Journals of Gerontology Series A: Biomedical Sciences and Medical SciencesOxford University Press

Published: Apr 28, 2018

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