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231225s2019 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2019.03.009
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|a eng
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|a Souliotis, Vassilis L
|e verfasserin
|4 aut
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| 245 |
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|a DNA damage accumulation, defective chromatin organization and deficient DNA repair capacity in patients with rheumatoid arthritis
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|c 2019
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|a Text
|b txt
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|a ƒaComputermedien
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|a ƒa Online-Ressource
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|a Date Completed 02.04.2020
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|a Date Revised 02.04.2020
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2019 Elsevier Inc. All rights reserved.
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|a We investigated the DNA damage response and repair network in 18 patients with active rheumatoid arthritis and tested the hypothesis that treatment influences this network. A 3-fold increase of endogenous DNA damage (single- and double-strand breaks) was detected in patient-derived peripheral blood mononuclear cells than controls (alkaline comet assay; mean ± SD Olive Tail Moment of 11.8 ± 7.3 versus 4.3 ± 2.2, p < .001). Patients exhibited significantly higher formation of DNA damage (oxidative stress and abasic sites), deficient global genome repair and more condensed chromatin structure than controls. Twelve weeks following treatment, chromatin structure loosened, global genome repair capacity was restored, oxidative stress and abasic sites decreased and levels of endogenous DNA damage reached control values in all 8 patients examined. We conclude that deregulated chromatin organization, deficient DNA repair capacity and augmented formation of DNA damage, which are reversible after treatment, contribute to the accumulation of endogenous DNA damage in rheumatoid arthritis
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a Antirheumatic treatment
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| 650 |
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|a Chromatin organization
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| 650 |
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|a DNA repair
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| 650 |
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|a Endogenous DNA damage
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| 650 |
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|a Oxidative stress
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| 650 |
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|a Rheumatoid arthritis
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| 650 |
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|a Chromatin
|2 NLM
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| 700 |
1 |
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|a Vlachogiannis, Nikolaos I
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Pappa, Maria
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Argyriou, Alexandra
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Sfikakis, Petros P
|e verfasserin
|4 aut
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| 773 |
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 203(2019) vom: 15. Juni, Seite 28-36
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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|g volume:203
|g year:2019
|g day:15
|g month:06
|g pages:28-36
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|u http://dx.doi.org/10.1016/j.clim.2019.03.009
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