NDLI: Phosphorylation of Histone H2AX in the Mouse Brain from Development to Senescence

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Phosphorylation of Histone H2AX in the Mouse Brain from Development to Senescence

Content Provider	MDPI
Author	Barral, Serena Beltramo, Riccardo Salio, Chiara Aimar, Patrizia Lossi, Laura Merighi, Adalberto
Abstract	Phosphorylation of the histone H2AX (γH2AX form) is an early response to DNA damage and a marker of aging and disease in several cells and tissues outside the nervous system. Little is known about in vivo phosphorylation of H2AX in neurons, although it was suggested that γH2AX is an early marker of neuronal endangerment thus opening the possibility to target it as a neuroprotective strategy. After experimental labeling of DNA-synthesizing cells with 5-bromo-2-deoxyuridine (BrdU), we studied the brain occurrence of γH2AX in developing, postnatal, adult and senescent (2 years) mice by light and electron microscopic immunocytochemistry and Western blotting. Focal and/or diffuse γH2AX immunostaining appears in interkinetic nuclei, mitotic chromosomes, and apoptotic nuclei. Immunoreactivity is mainly associated with neurogenetic areas, i.e., the subventricular zone (SVZ) of telencephalon, the cerebellar cortex, and, albeit to a much lesser extent, the subgranular zone of the hippocampal dentate gyrus. In addition, γH2AX is highly expressed in the adult and senescent cerebral cortex, particularly the piriform cortex. Double labeling experiments demonstrate that γH2AX in neurogenetic brain areas is temporally and functionally related to proliferation and apoptosis of neuronal precursors, i.e., the type C transit amplifying cells (SVZ) and the granule cell precursors (cerebellum). Conversely, γH2AX-immunoreactive cortical neurons incorporating the S phase-label BrdU do not express the proliferation marker phosphorylated histone H3, indicating that these postmitotic cells undergo a significant DNA damage response. Our study paves the way for a better comprehension of the role of H2AX phosphorylation in the normal brain, and offers additional data to design novel strategies for the protection of neuronal precursors and mature neurons in central nervous system (CNS) degenerative diseases.
File Size	2837504
Ending Page	1573
Page Count	20
Starting Page	1554
File Format	PDF
e-ISSN	14220067
DOI	10.3390/ijms15011554
Journal	International Journal of Molecular Sciences
Issue Number	1
Volume Number	15
Language	English
Publisher Date	2014-01-21
Access Restriction	Open
Subject Keyword	H2AX histone DNA damage immunocytochemistry cell proliferation apoptosis neuroprotection Alzheimer’s disease Huntington’s disease
Content Type	Text
Resource Type	Article

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