DNA damage-induced cell death: lessons from the central nervous system

Borges, Helena L.; Linden, Rafael; Wang, Jean Y. J.

doi:10.1038/cr.2007.110

Cited by 132 publications

(98 citation statements)

References 78 publications

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“…We found that cell death depended on incubation time after UV irradiation, and cell death after irradiation was not significantly reduced until 24 h at all wavelengths. Cell death occurs from irreparable DNA damage that remains 24-48 h after UV exposure [19,40].…”

Section: Introduction Introduction Introduction Introductionmentioning

confidence: 99%

Effects of UV wavelength on cell damages caused by UV irradiation in PC12 cells

Masuma

Kashima

Kurasaki

et al. 2013

Journal of Photochemistry and Photobiology B: Biology

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Ultraviolet (UV) radiations present in sunlight are a major etiologic factor for many skin diseases and induce DNA damage through formation of cyclobutane pyrimidine dimer (CPD). This study was conducted to determine the toxicological effects of different wavelengths (250, 270, 290, and 310 nm) and doses of UV radiation on cell viability, DNA structure, and DNA damage repair mechanisms in a PC12 cell system. For this, we evaluated cell viability and CPD formation. Cell survival rate was markedly decreased 24 h after UV irradiation in a dose-dependent manner at all wavelengths (except at 310 nm). Cell viability increased with increasing wavelength in the following order: 250 < 270 < 290 < 310 nm. UV radiation at 250 nm showed the highest cell killing ability, with a median lethal dose (LD50) of 120 mJ/cm2. The LD50 gradually increased with increase in wavelength. Among the 4 wavelengths tested, the highest LD50 (6000 mJ/cm2) was obtained for 310 nm. CPD formation decreased substantially with increasing wavelength. Among the 4 wavelengths, the proportion of CPD formation was highest at 250 nm and lowest at 310 nm. On the basis of LD50 values for each wavelength, PC12 cells irradiated with UV radiation of 290 nm showed maximum DNA repair ability, whereas those irradiated with the 310-nm radiation did not show any repair ability. Toxicity of UV radiation varied with wavelengths and exposure doses

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Section: Introduction Introduction Introduction Introductionmentioning

confidence: 99%

Effects of UV wavelength on cell damages caused by UV irradiation in PC12 cells

Masuma

Kashima

Kurasaki

et al. 2013

Journal of Photochemistry and Photobiology B: Biology

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“…In animals, cell death downstream of ATM or ATR activation is usually mediated by p53 and occurs through apoptosis (13,30). Plants do not have recognizable homologs of p53 or core regulators and executioners of apoptosis, such as APAF1, BCL2, or caspases (19).…”

Section: Programmed Death After Dna Damage Showed Autolytic Rather Thanmentioning

confidence: 99%

Hypersensitivity to DNA damage in plant stem cell niches

Fulcher

Sablowski

2009

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

236

243

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The growing apices of plants contain stem cells that continually produce tissues, which, in the shoot, include the germline. These stem cell populations remain active throughout the plant's life, which can last for centuries, and are particularly exposed to environmental hazards that cause DNA damage and mutations. It is not known whether plants have mechanisms to safeguard the genome specifically in these crucial cell populations. Here, we show that root and shoot stem cells and their early descendants are selectively killed by mild treatment with radiomimetic drugs, x-rays, or mutations that disrupt DNA repair by nonhomologous end-joining. Stem cell death required transduction of DNA damage signals by the ATAXIA-TELANGIECTASIA MUTATED (ATM) kinase and, specifically in the root, also the ATM/RAD3-RELATED (ATR) kinase. Consistent with the absence of p53 and the core apoptotic machinery in plants, death of the stem cells did not show apoptotic but autolytic features as seen in other cases of plant developmentally programmed cell death. We propose that plants have independently evolved selective death as a stringent mechanism to safeguard genome integrity in their stem cell populations.Arabidopsis ͉ double-strand breaks ͉ meristem ͉ programmed cell death

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“…Conformational changes of DNA, manifested as double-strand breaks, mispairings, or modifications in the nucleosides, can be related to diseases, ageing or cell death [1][2][3][4] . One way to detect these conformational changes is by employing electron paramagnetic resonance (EPR) techniques which can provide structural information [5][6][7][8] .…”

Section: Introductionmentioning

confidence: 99%

π-Stacking effects on the EPR parameters of a prototypical DNA spin label

Frecuş

Rinkevičius

Ågren

2013

Phys. Chem. Chem. Phys.

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The character and value of spin labels for probing environments like double-stranded DNA depends on the degree of change of the spin Hamiltonian parameters of the spin label induced by the environment. Herein we provide a systematic theoretical investigation of this issue, based on a density functional theory method applied to a spin labeled DNA model system, focusing on the dependence of the EPR properties of the spin label on the π stacking and hydrogen bonding that occur upon incorporating the spin label into selected base pair inside DNA. It is found that the EPR spin Hamiltonian parameters of the spin label is only negligibly affected by its incorporation into DNA, when compared to the its free form. This result gives theoretical ground for the common empirical assumption regarding the behaviour of spin Hamiltonian parameters made in EPR based measurements of distance between spin labels incorporated into DNA.

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DNA damage-induced cell death: lessons from the central nervous system

Cited by 132 publications

References 78 publications

Effects of UV wavelength on cell damages caused by UV irradiation in PC12 cells

Effects of UV wavelength on cell damages caused by UV irradiation in PC12 cells

Hypersensitivity to DNA damage in plant stem cell niches

π-Stacking effects on the EPR parameters of a prototypical DNA spin label

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