Locating and labeling neural stem cells in the brain

Landgren, Henrik; Curtis, Maurice A.

doi:10.1002/jcp.22319

Cited by 54 publications

(54 citation statements)

References 103 publications

(124 reference statements)

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“…During the last few years, new markers to monitor gliogenesis and neurogenesis in the adult DG have been discovered and successfully introduced. A major problem in studies of adult neurogenesis is currently the lack of a unique marker defining adult neural stem cells (Landgren and Curtis 2011). Stem cells express many genes that are also expressed by astrocytes (Doetsch 2003;Garcia et al 2004).…”

Section: Perspectivesmentioning

confidence: 99%

Immunohistological markers for proliferative events, gliogenesis, and neurogenesis within the adult hippocampus

2011

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Biologists long believed that, once development is completed, no new neurons are produced in the forebrain. However, as is now firmly established, new neurons can be produced at least in two specific forebrain areas: the subventricular zone (SVZ) and the dentate gyrus (DG) of the hippocampal formation. Neurogenesis within the adult DG occurs constitutively throughout postnatal life, and the rate of neurogenesis within the DG can be altered under various physiological and pathophysiological conditions. The process of adult neurogenesis within the DG is a multi-step process (proliferation, differentiation, migration, targeting, and synaptic integration) that ends with the formation of a post-mitotic functionally integrated new neuron. Various markers are expressed during specific stages of adult neurogenesis. The availability of such markers allows the time-course and fate of newly born cells to be followed within the DG in a detailed and precise fashion. Several of the available markers (e.g., PCNA, Ki-67, PH3, MCM2) are markers for proliferative events, whereas others are more specific for early phases of neurogenesis and gliogenesis within the adult DG (e.g., nestin, GFAP, Sox2, Pax6). In addition, markers are available allowing events to be distinguished that are related to later steps of gliogenesis (e.g., vimentin, BLBP, S100beta) or neurogenesis (e.g., NeuroD, PSA-NCAM, DCX).

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Section: Perspectivesmentioning

confidence: 99%

Immunohistological markers for proliferative events, gliogenesis, and neurogenesis within the adult hippocampus

2011

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“…Firstly, damaged cortical cells may undergo a number of DNA repair processes after stroke, which could incorporate BrdU into already mature, cortical cells (Landgren and Curtis, 2010). Secondly, some evidence suggests that mature astrocytes, already localized in the cortex, may actually change their cellular fate in response to ischemia, such that they take on a neuronal phenotype (Landgren and Curtis, 2010).…”

Section: Cellular Changesmentioning

confidence: 99%

Thinning, movement, and volume loss of residual cortical tissue occurs after stroke in the adult rat as identified by histological and magnetic resonance imaging analysis

et al. 2010

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“…In the late postnatal and adult brain, newborn neurons arise from neural stem/progenitor cells (NSPCs) in both the subgranular zone (SGZ) of the hippocampal dentate gyrus and in the subventricular zone (SVZ) (6). We previously reported a discrete expression pattern of Neil3 in the rodent SGZ and SVZ, confined to the embryonic and perinatal stages (7,8).…”

mentioning

confidence: 99%

Endonuclease VIII-like 3 (Neil3) DNA glycosylase promotes neurogenesis induced by hypoxia-ischemia

Sejersted¹,

Hildrestrand²,

Kunke³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

127

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Neural stem/progenitor cell proliferation and differentiation are required to replace damaged neurons and regain brain function after hypoxic-ischemic events. DNA base lesions accumulating during hypoxic-ischemic stress are removed by DNA glycosylases in the base-excision repair pathway to prevent cytotoxicity and mutagenesis. Expression of the DNA glycosylase endonuclease VIII-like 3 (Neil3) is confined to regenerative subregions in the embryonic and perinatal brains. Here we show profound neuropathology in Neil3-knockout mice characterized by a reduced number of microglia and loss of proliferating neuronal progenitors in the striatum after hypoxia-ischemia. In vitro expansion of Neil3-deficient neural stem/progenitor cells revealed an inability to augment neurogenesis and a reduced capacity to repair for oxidative base lesions in single-stranded DNA. We propose that Neil3 exercises a highly specialized function through accurate molecular repair of DNA in rapidly proliferating cells.DNA damage | formamidopyrimidine-DNA glycosylase/endonuclease VIII | hydantoins | neural stem cells | neuronal progenitor cells T he base-excision repair pathway (BER) maintains genomic integrity by removing base lesions caused by oxidation, alkylation, and deamination. DNA base lesions frequently are cytotoxic or mutagenic if not removed. BER is initiated by DNA glycosylases that recognize modified bases and catalyze cleavage of the N-glycosidic bond, creating an apurinic or apyrimidinic (AP) site. The exposed DNA backbone is cleaved by the AP lyase activity of bifunctional DNA glycosylases or by an AP endonuclease. Repair synthesis is completed by gap filling and ligation (1, 2).Endonuclease VIII-like 3 (NEIL3) and endonuclease VIII-like 1 (NEIL1) are mammalian oxidized base-specific DNA glycosylases (3, 4). The function of NEIL3 has remained enigmatic, but recently the mouse ortholog was shown to remove a broad spectrum of oxidative base lesions on single-stranded DNA substrates with preference for spiroiminodihydantoin (Sp) and guanidinohydantoin (Gh), which are further oxidation products of one of the most common base lesions, 8-oxo-7,8-dihydroguanine (8ohG) (5). These findings suggest that NEIL3 serves as a DNA glycosylase to prevent accumulation of cytotoxic and mutagenic DNA lesions in mammalian cells, although the activity of NEIL1 far exceeds that of NEIL3 on most substrates.In the late postnatal and adult brain, newborn neurons arise from neural stem/progenitor cells (NSPCs) in both the subgranular zone (SGZ) of the hippocampal dentate gyrus and in the subventricular zone (SVZ) (6). We previously reported a discrete expression pattern of Neil3 in the rodent SGZ and SVZ, confined to the embryonic and perinatal stages (7,8). These observations indicate a role for Neil3 in proliferating cells in the brain. However, naïve Neil3-knockout mice generated by us and others (4) appear phenotypically normal. After perinatal hypoxic-ischemic (HI) and adult ischemic stroke, proliferation of SVZ NSPCs is enhanced, and differentiating p...

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Locating and labeling neural stem cells in the brain

Cited by 54 publications

References 103 publications

Immunohistological markers for proliferative events, gliogenesis, and neurogenesis within the adult hippocampus

Immunohistological markers for proliferative events, gliogenesis, and neurogenesis within the adult hippocampus

Thinning, movement, and volume loss of residual cortical tissue occurs after stroke in the adult rat as identified by histological and magnetic resonance imaging analysis

Endonuclease VIII-like 3 (Neil3) DNA glycosylase promotes neurogenesis induced by hypoxia-ischemia

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