期刊论文详细信息
BMC Geriatrics
PML-nuclear bodies decrease with age and their stress response is impaired in aged individuals
Luitpold V Distel2  Rainer Fietkau2  Manfred Schmidt2  Christoph Daniel1  Maria Brunner2  Manuela Schwegler2  Barbara Wenger2 
[1] Institute of Pathology, Department of Nephropathology, University Hospitals and Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany;Department of Radiation Oncology, University Hospitals and Friedrich-Alexander-University Erlangen-Nürnberg, Universitätsstraße 27, D-91054 Erlangen, Germany
关键词: Senescence;    Stress response;    γH2AX;    PML Nuclear bodies;    Aging;   
Others  :  855188
DOI  :  10.1186/1471-2318-14-42
 received in 2013-11-29, accepted in 2014-03-26,  发布年份 2014
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【 摘 要 】

Background

Promyelocytic 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.

Methods

In 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.

Results

The 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.

Conclusion

The findings suggest that there is a dysfunctional PML-NBs stress response in aged cells.

【 授权许可】

   
2014 Wenger et al.; licensee BioMed Central Ltd.

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