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Low-Dose/Dose-Rate gamma Radiation Depresses Neural Differentiation and Alters Protein Expression Profiles in Neuroblastoma SH-SY5Y Cells and C17.2 Neural Stem Cells
Stockholms universitet, Naturvetenskapliga fakulteten, Institutionen för genetik, mikrobiologi och toxikologi.
Stockholms universitet, Naturvetenskapliga fakulteten, Institutionen för neurokemi.
Stockholms universitet, Naturvetenskapliga fakulteten, Institutionen för neurokemi.
Stockholms universitet, Naturvetenskapliga fakulteten, Institutionen för genetik, mikrobiologi och toxikologi.
Vise andre og tillknytning
2011 (engelsk)Inngår i: Radiation Research, ISSN 0033-7587, E-ISSN 1938-5404, Vol. 175, nr 2, s. 185-192Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

The effects of low doses of ionizing radiation on cellular development in the nervous system are presently unclear. The focus of the present study was to examine low-dose gamma-radiation-induced effects on the differentiation of neuronal cells and on the development of neural stem cells to glial cells. Human neuroblastoma SH-SY5Y cells were exposed to (137)Cs gamma rays at different stages of retinoic acid-induced neuronal differentiation, and neurite formation was determined 6 days after exposure. When SH-SY5Y cells were exposed to low-dose-rate gamma rays at the onset of differentiation, the number of neurites formed per cell was significantly less after exposure to either 10, 30 or 100 mGy compared to control cells. Exposure to 10 and 30 mGy attenuated differentiation of immature C17.2 mouse-derived neural stem cells to glial cells, as verified by the diminished expression of glial fibrillary acidic protein. Proteomic analysis of the neuroblastoma cells by 2D-PAGE after 30 mGy irradiation showed that proteins involved in neuronal development were downregulated. Proteins involved in cell cycle and proliferation were altered in both cell lines after exposure to 30 mGy; however, the rate of cell proliferation was not affected in the low-dose range. The radiation-induced attenuation of differentiation and the persistent changes in protein expression is indicative of an epigenetic rather than a cytotoxic mechanism. (C) 2011 by Radiation Research Society

sted, utgiver, år, opplag, sider
2011. Vol. 175, nr 2, s. 185-192
HSV kategori
Identifikatorer
URN: urn:nbn:se:su:diva-67348DOI: 10.1667/RR2090.1ISI: 000287113500006OAI: oai:DiVA.org:su-67348DiVA, id: diva2:470259
Merknad
authorCount :5Tilgjengelig fra: 2011-12-28 Laget: 2011-12-28 Sist oppdatert: 2017-12-08bibliografisk kontrollert
Inngår i avhandling
1. Studies of DNA repair strategies in response to complex DNA damages
Åpne denne publikasjonen i ny fane eller vindu >>Studies of DNA repair strategies in response to complex DNA damages
2012 (engelsk)Doktoravhandling, med artikler (Annet vitenskapelig)
Abstract [en]

The main aim of this thesis was to study the role of the indirect actions of γ-rays and α-particles on the complexity of primary DNA damages and the repair fidelity of major DNA repair pathways: non-homologous end joining (NHEJ), homologous recombination repair (HRR) and base excision repair (BER). The complexity of radiation-induced damages increases and the proximity between damages decreases with increasing LET due to formation of ionization clusters along the particle track. The complexity of damages formed can be modified by the free radical scavenger dimethyl sulfoxide (DMSO). In addition, the effects of low doses of low dose rate γ-radiation on cellular response in terms of differentiation were investigated.

Paper I investigates the role of the indirect effect of radiation on repair fidelity of HRR, NHEJ and BER when damages of different complexity were induced by radiation or by potassium bromate. We found that potassium bromate induces complex DNA damages through processing of base modifications and that the indirect effect of radiation has a high impact on the NHEJ pathway. Results in paper II confirmed our conclusions in paper I that the indirect effect from both γ-rays and α-particles has an impact on all three repair pathways studied and NHEJ benefits the most when the indirect effect of radiation is removed.

In paper III we investigated the effects of low dose/dose rate γ-radiation on the developmental process of neural cells by using cell models for neurons and astrocytes. Our results suggest that low dose/dose rate γ-radiation attenuates differentiation and down-regulates proteins involved in the differentiation process of neural cells by an epigenetic rather than cytotoxic mechanism.

sted, utgiver, år, opplag, sider
Department of Genetics, Microbiology and Toxicology, Stockholm University, 2012. s. 41
Emneord
ionizing radiation, complex DNA damage, indirect effect of radiation, dimethyl sulfoxide
HSV kategori
Forskningsprogram
molekylärgenetik
Identifikatorer
urn:nbn:se:su:diva-72472 (URN)978-91-7447-456-5 (ISBN)
Disputas
2012-03-23, Magnélisalen, Kemiska övningslaboratoriet, Svante Arrhenius väg 16 B, Stockholm, 10:00 (engelsk)
Opponent
Veileder
Merknad

At the time of doctoral defense, the following paper was unpublished and had a status as follows: Paper 2: Manuscript.

Tilgjengelig fra: 2012-03-01 Laget: 2012-02-13 Sist oppdatert: 2018-10-12bibliografisk kontrollert

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