PML-nuclear bodies decrease with age and their stress response is impaired in aged individuals

BMC Geriatrics

Research Article

Barbara Wenger¹  Maria Brunner¹  Manfred Schmidt¹  Rainer Fietkau¹  Manuela Schwegler¹  Luitpold V Distel¹  Christoph Daniel² 

[1] Department of Radiation Oncology, University Hospitals and Friedrich-Alexander-University Erlangen-Nürnberg, Universitätsstraße 27, D-91054, Erlangen, Germany;Institute of Pathology, Department of Nephropathology, University Hospitals and Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany;

关键词: Aging;    PML Nuclear bodies;    γH2AX;    Stress response;    Senescence;   

DOI  :  10.1186/1471-2318-14-42

 received in 2013-11-29, accepted in 2014-03-26,  发布年份 2014

来源: Springer

【 摘 要 】

BackgroundPromyelocytic leukemia nuclear bodies (PML-NBs) have been depicted as structures which are involved in processing cell damages and DNA double-strand break repairs. The study was designed to evaluate differences in patients’ PML-NBs response to stress factors like a cancerous disease and ionizing radiation exposure dependent on age.MethodsIn order to clarify the role of PML-NBs in the aging process, we examined peripheral blood monocytes of 134 cancer patients and 41 healthy individuals between 22 and 92 years of age, both before and after in vitro irradiation. Additionally, we analyzed the samples of the cancer patients after in vivo irradiation. Cells were immunostained and about 1600 cells per individual were analyzed for the presence of PML- and γH2AX foci.ResultsThe number of existing PML-NBs per nucleus declined with age, while the number of γH2AX foci increased with age. There was a non-significant trend that in vivo irradiation increased the number of PML-NBs in cells of young study participants, while in older individuals PML-NBs tended to decrease. It can be assumed that PML-NBs decrease in number during the process of aging.ConclusionThe findings suggest that there is a dysfunctional PML-NBs stress response in aged cells.

【 授权许可】

Unknown   
© Wenger et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.