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Int. J. Mol. Sci. 2015, 16(8), 17422-17444; doi:10.3390/ijms160817422

Combination of Aβ Secretion and Oxidative Stress in an Alzheimer-Like Cell Line Leads to the Over-Expression of the Nucleotide Excision Repair Proteins DDB2 and XPC

Laboratoire Lésions des Acides Nucléiques, Université Joseph Fourier-Grenoble 1/CEA/Institut Nanoscience et Cryogénie/SCIB, UMR-E3, Grenoble, France
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Academic Editor: G. Jean Harry
Received: 7 May 2015 / Revised: 19 June 2015 / Accepted: 29 June 2015 / Published: 30 July 2015
(This article belongs to the Special Issue Molecular Research in Neurotoxicology)
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Abstract

Repair of oxidative DNA damage, particularly Base Excision Repair (BER), impairment is often associated with Alzheimer’s disease pathology. Here, we aimed at investigating the complete Nucleotide Excision Repair (NER), a DNA repair pathway involved in the removal of bulky DNA adducts, status in an Alzheimer-like cell line. The level of DNA damage was quantified using mass spectrometry, NER gene expression was assessed by qPCR, and the NER protein activity was analysed through a modified version of the COMET assay. Interestingly, we found that in the presence of the Amyloid β peptide (Aβ), NER factors were upregulated at the mRNA level and that NER capacities were also specifically increased following oxidative stress. Surprisingly, NER capacities were not differentially improved following a typical NER-triggering of ultraviolet C (UVC) stress. Oxidative stress generates a differential and specific DNA damage response in the presence of Aβ. We hypothesized that the release of NER components such as DNA damage binding protein 2 (DDB2) and Xeroderma Pigmentosum complementation group C protein (XPC) following oxidative stress might putatively involve their apoptotic role rather than DNA repair function. View Full-Text
Keywords: neurodegenerative disorders; Alzheimer’s disease; DNA damage; DNA repair; nucleotide excision repair; XPC; DDB2; oxidative stress neurodegenerative disorders; Alzheimer’s disease; DNA damage; DNA repair; nucleotide excision repair; XPC; DDB2; oxidative stress
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MDPI and ACS Style

Forestier, A.; Douki, T.; De Rosa, V.; Béal, D.; Rachidi, W. Combination of Aβ Secretion and Oxidative Stress in an Alzheimer-Like Cell Line Leads to the Over-Expression of the Nucleotide Excision Repair Proteins DDB2 and XPC. Int. J. Mol. Sci. 2015, 16, 17422-17444.

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