scholarly journals An Enriched Environment Alters DNA Repair and Inflammatory Responses After Radiation Exposure

2021 ◽  
Vol 12 ◽  
Author(s):  
Sae Sakama ◽  
Keisuke Kurusu ◽  
Mayu Morita ◽  
Takashi Oizumi ◽  
Shinya Masugata ◽  
...  
Keyword(s):  
Dna Damage ◽  
Inflammatory Response ◽  
Radiation Exposure ◽  
Dna Damage Response ◽  
Inflammatory Responses ◽  
Enriched Environment ◽  
Physical And Mental Health ◽  
Chronic Inflammatory Response ◽  
Damage Response ◽  
Radiation Induced

After the Fukushima Daiichi Nuclear Power Plant accident, there is growing concern about radiation-induced carcinogenesis. In addition, living in a long-term shelter or temporary housing due to disasters might cause unpleasant stress, which adversely affects physical and mental health. It’s been experimentally demonstrated that “eustress”, which is rich and comfortable, has beneficial effects for health using mouse models. In a previous study, mice raised in the enriched environment (EE) has shown effects such as suppression of tumor growth and enhancement of drug sensitivity during cancer treatment. However, it’s not yet been evaluated whether EE affects radiation-induced carcinogenesis. Therefore, to evaluate whether EE suppresses a radiation-induced carcinogenesis after radiation exposure, in this study, we assessed the serum leptin levels, radiation-induced DNA damage response and inflammatory response using the mouse model. In brief, serum and tissues were collected and analyzed over time in irradiated mice after manipulating the raising environment during the juvenile or adult stage. To assess the radiation-induced DNA damage response, we performed immunostaining for phosphorylated H2AX which is a marker of DNA double-strand break. Focusing on the polarization of macrophages in the inflammatory reaction that has an important role in carcinogenesis, we performed analysis using tissue immunofluorescence staining and RT-qPCR. Our data confirmed that EE breeding before radiation exposure improved the responsiveness to radiation-induced DNA damage and basal immunity, further suppressing the chronic inflammatory response, and that might lead to a reduction of the risk of radiation-induced carcinogenesis.

scholarly journals Polymorphisms of DNA damage response genes in radiation-related and sporadic papillary thyroid carcinoma

2009 ◽  
Vol 16 (2) ◽  
pp. 491-503 ◽  
Author(s):  
Natallia M Akulevich ◽  
Vladimir A Saenko ◽  
Tatiana I Rogounovitch ◽  
Valentina M Drozd ◽  
Eugeny F Lushnikov ◽  
...  
Keyword(s):  
Dna Damage ◽  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Radiation Exposure ◽  
Dna Damage Response ◽  
Papillary Thyroid ◽  
Retrospective Case ◽  
Increased Risk ◽  
Damage Response ◽  
Radiation Induced

Papillary thyroid carcinoma (PTC) etiologically occurs as a radiation-induced or sporadic malignancy. Genetic factors contributing to the susceptibility to either form remain unknown. In this retrospective case–control study, we evaluated possible associations between single-nucleotide polymorphisms (SNPs) in the candidate DNA damage response genes (ATM, XRCC1, TP53, XRCC3, MTF1) and risk of radiation-induced and sporadic PTC. A total of 255 PTC cases (123 Chernobyl radiation-induced and 132 sporadic, all in Caucasians) and 596 healthy controls (198 residents of Chernobyl areas and 398 subjects without history of radiation exposure, all Caucasians) were genotyped. The risk of PTC and SNPs interactions with radiation exposure were assessed by logistic regressions. The ATM G5557A and XRCC1 Arg399Gln polymorphisms, regardless of radiation exposure, associated with a decreased risk of PTC according to the multiplicative and dominant models of inheritance (odds ratio (OR)=0.69, 95% confidence interval (CI) 0.45–0.86 and OR=0.70, 95% CI 0.59–0.93 respectively). The ATM IVS22-77 T>C and TP53 Arg72Pro SNPs interacted with radiation (P=0.04 and P=0.01 respectively). ATM IVS22-77 associated with the increased risk of sporadic PTC (OR=1.84, 95% CI 1.10–3.24) whereas TP53 Arg72Pro correlated with the higher risk of radiogenic PTC (OR=1.80, 95% CI 1.06–2.36). In the analyses of ATM/TP53 (rs1801516/rs664677/rs609429/rs1042522) combinations, the GG/TC/CG/GC genotype strongly associated with radiation-induced PTC (OR=2.10, 95% CI 1.17–3.78). The GG/CC/GG/GG genotype displayed a significantly increased risk for sporadic PTC (OR=3.32, 95% CI 1.57–6.99). The results indicate that polymorphisms of DNA damage response genes may be potential risk modifiers of ionizing radiation-induced or sporadic PTCs.

Radiation-induced DNA damage response and resistance in colorectal cancer stem-like cells

2019 ◽  
Vol 95 (6) ◽  
pp. 667-679 ◽  
Author(s):  
Kumari Anuja ◽  
Amit Roy Chowdhury ◽  
Arka Saha ◽  
Souvick Roy ◽  
Arabinda Kumar Rath ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Dna Damage ◽  
Dna Damage Response ◽  
Damage Response ◽  
Radiation Induced

Ionizing radiation-induced DNA damage response identified in marine mussels, Mytilus sp.

2012 ◽  
Vol 168 ◽  
pp. 107-112 ◽  
Author(s):  
Ohoud D. AlAmri ◽  
Andrew B. Cundy ◽  
Yanan Di ◽  
Awadhesh N. Jha ◽  
Jeanette M. Rotchell
Keyword(s):  
Dna Damage ◽  
Ionizing Radiation ◽  
Dna Damage Response ◽  
Damage Response ◽  
Marine Mussels ◽  
Radiation Induced

scholarly journals Nucleic Acid Immunity and DNA Damage Response: New Friends and Old Foes

2021 ◽  
Vol 12 ◽  
Author(s):  
Clara Taffoni ◽  
Alizée Steer ◽  
Johanna Marines ◽  
Hanane Chamma ◽  
Isabelle K. Vila ◽  
...  
Keyword(s):  
Dna Damage ◽  
Nucleic Acid ◽  
Nucleic Acids ◽  
Dna Damage Response ◽  
Immune Activation ◽  
Inflammatory Responses ◽  
Innate Immune ◽  
Fine Tuning ◽  
Innate Immune Activation ◽  
Damage Response

The maintenance of genomic stability in multicellular organisms relies on the DNA damage response (DDR). The DDR encompasses several interconnected pathways that cooperate to ensure the repair of genomic lesions. Besides their repair functions, several DDR proteins have emerged as involved in the onset of inflammatory responses. In particular, several actors of the DDR have been reported to elicit innate immune activation upon detection of cytosolic pathological nucleic acids. Conversely, pattern recognition receptors (PRRs), initially described as dedicated to the detection of cytosolic immune-stimulatory nucleic acids, have been found to regulate DDR. Thus, although initially described as operating in specific subcellular localizations, actors of the DDR and nucleic acid immune sensors may be involved in interconnected pathways, likely influencing the efficiency of one another. Within this mini review, we discuss evidences for the crosstalk between PRRs and actors of the DDR. For this purpose, we mainly focus on cyclic GMP-AMP (cGAMP) synthetase (cGAS) and Interferon Gamma Inducible Protein 16 (IFI16), as major PRRs involved in the detection of aberrant nucleic acid species, and components of the DNA-dependent protein kinase (DNA-PK) complex, involved in the repair of double strand breaks that were recently described to qualify as potential PRRs. Finally, we discuss how the crosstalk between DDR and nucleic acid-associated Interferon responses cooperate for the fine-tuning of innate immune activation, and therefore dictate pathological outcomes. Understanding the molecular determinants of such cooperation will be paramount to the design of future therapeutic approaches.

scholarly journals Analysis of DNA damage response following proton radiation exposure in an in vitro neuronal model

2021 ◽  
Author(s):  
Mihaela Temelie ◽  
Tiberiu Esanu ◽  
Liviu Craciun ◽  
Nicoleta Moisoi ◽  
Diana Savu
Keyword(s):  
Dna Damage ◽  
Radiation Exposure ◽  
Dna Damage Response ◽  
Neuronal Model ◽  
Proton Radiation ◽  
Damage Response
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