Abstract
P53 and its family member p63 play important roles in cellular senescence and organismal aging. In this study, p53 and p63 immunoreactivity were examined in the hippocampus of young, adult and aged mice by using immunohistochemistry. In addition, neuronal distribution and degeneration was examined by NeuN immunohistochemistry and fluoro-Jade B fluorescence staining. Strong p53 immunoreactivity was mainly expressed in pyramidal and granule cells of the hippocampus in young mice. p53 immunoreactivity in the pyramidal and granule cells was significantly reduced in the adult mice. In the aged mice, p53 immunoreactivity in the pyramidal and granule cells was more significantly decreased. p63 immunoreactivity was strong in the pyramidal and granule cells in the young mice. p63 immunoreactivity in these cells was apparently and gradually decreased with age, showing that p63 immunoreactivity in the aged granule cells was hardly shown. However, numbers of pyramidal neurons and granule cells were not significantly decreased in the aged mice with normal aging. Taken together, this study indicates that there are no degenerative neurons in the hippocampus during normal aging, showing that p53 and p63 immunoreactivity in hippocampal neurons was progressively reduced during normal aging, which might be closely related to the normal aging processes.
Highlights
The p53 gene family is composed of a group of transcription factors including a key tumor suppressor p53, and its homologs p63 and p73 [1, 2]
In this study, we examined p53, p63 and NeuN immunoreactivity, and Fluoro-jade B (F-J B) histofluorescence in the hippocampus proper, which consists of Cornu Ammonis 1–3 subfields (CA1–3), and in the dentate gyrus
P53 immunoreactivity CA1–3 In the young group, strong p53 immunoreactivity was detected in pyramidal cells, which consist of the stratum pyramidale, and in non-pyramidal cells, which are located in the stratum oriens and radiatum (Fig. 1 A, D, G)
Summary
The p53 gene family is composed of a group of transcription factors including a key tumor suppressor p53, and its homologs p63 and p73 [1, 2]. It has widely been reported that the majority of human cancers show mutations that abrogate p53 network which is related to many antiproliferative cellular responses in context-dependent manner [3,4,5]. In rodent and human brains, p53 and p63 expressions have been reported. Researches on the activity of p53 or p63 in noncancer (normal) tissues in response to cerebral ischemia have been examined [9,10,11]. Aging is defined as progressive decline of normal body functions necessary for survival and reproduction accompanied by accumulation of deleterious changes (molecular and cellular damages) that result in increased risk of diseases and death [12]. The loss of maintenance of DNA integrity contributes to the onset of cellular senescence or cell death, and this genomic instability is caused by oxidative stress, genotoxic drugs and replication errors [2]
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