In vitro exposure of human lens epithelial cells to X-rays at varied dose-rates leads to protein-level changes relevant to cataractogenesis

Chauhan, Vinita; Vuong, Ngoc Q.; Bahia, Simran; Nazemof, Nazila; Kumarathasan, Premkumari

doi:10.1080/09553002.2020.1846819

Cited by 4 publications

(3 citation statements)

References 40 publications

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“…Radiation exposure could damage the lens epithelial cells of the eye to induce cataracts [ 40 , 41 ]. We thus examined whether irradiation could injure retinal cells to give rise to AMD.…”

Section: Resultsmentioning

confidence: 99%

LncRNA NORAD defects deteriorate the formation of age-related macular degeneration

Zhang

Jiang

Zhou

et al. 2023

Aging

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Long noncoding RNAs (lncRNAs) play important roles in the development of age-related macular degeneration (AMD). However, the effect of long non-coding RNA activated by DNA damage (NORAD) on AMD remains unknown. This study aimed to investigate the effect of NORAD on RPE cell senescence and degeneration. Irradiated adult retinal pigment epithelial cell line-19 (ARPE-19) and sodium iodate-treated mice were used as in vitro and in vivo AMD models. Results showed that irradiation-induced AMD characteristics of ARPE-19 and NORAD-knockdown aggravated cell cycle arrest in the G2/M phase, cell apoptosis and cell senescence along with the increased expression of phosphorylated P53 (p-P53) and P21. AMD factors C3, ICAM-1, APP, APOE, and VEGF-A were also increased by NORAD-knockdown. Moreover, NORAD-knockdown increased irradiation-induced reduction of mitochondrial homeostasis factors, (i.e., TFAM and POLG) and mitochondrial respiratory chain complex genes (i.e., ND1 and ND5) along with mitochondrial reactive oxygen species (ROS). We also identified a strong interaction of NORAD and PGC-1α and sirtuin 1 (SIRT1) in ARPE-19; that is, NORAD knockdown increases the acetylation of PGC-1α. In NORAD knockout mice, NORAD-knockout accelerated the sodium iodate-reduced retinal thickness reduction, function impairment and loss of retinal pigment in the fundus. Therefore, NORAD-knockdown accelerates retinal cell senescence, apoptosis, and AMD markers via PGC-1α acetylation, mitochondrial ROS, and the p-P53–P21signaling pathway, in which NORAD-mediated effect on PGC-1α acetylation might occur through the direct interaction with PGC-1α and SIRT1.

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“…Radiation exposure could damage the lens epithelial cells of the eye to induce cataracts [ 40 , 41 ]. We thus examined whether irradiation could injure retinal cells to give rise to AMD.…”

Section: Resultsmentioning

confidence: 99%

LncRNA NORAD defects deteriorate the formation of age-related macular degeneration

Zhang

Jiang

Zhou

et al. 2023

Aging

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“…Part 2 was on "Epidemiology: Updates on epidemiological low dose studies", co-chaired by Cato M. Milder and Mark P. Little (Milder et al 2021). This second Bill Morgan Special Issue consists of two meeting reports (Laiakis et al 2021;Milder et al 2021), four review articles highlighted from recorded presentations in parts 1 and 2 (Chauhan et al 2021b;Kendall et al 2021;Little et al 2021;Paunesku et al 2021), three original articles (Chauhan et al 2021a;Golden et al 2021;Karpov et al 2021) and one review article (Preston et al 2021). give an overview of NCRP Report No.…”

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confidence: 99%

“…In this Special Issue,Paunesku et al (2021) give an overview regarding cancer effects of low dose and low dose rate low linear energy transfer (low-LET) radiation in animal models Chauhan et al (2021a). report protein level changes in human lens epithelial cells exposed to X-rays at various dose rates Kendall et al (2021).…”

mentioning

confidence: 99%

Introduction to the Second Bill Morgan Memorial Special Issue: an update on low dose biology, epidemiology, its integration and implications for radiation protection

Hamada

Laiakis

Zablotska

et al. 2021

International Journal of Radiation Biology

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Bringing together scientific disciplines for collaborative undertakings: a vision for advancing the adverse outcome pathway framework

Chauhan

Wilkins

Beaton

et al. 2021

International Journal of Radiation Biology

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Background: Decades of research to understand the impacts of various types of environmental occupational and medical stressors on human health have produced a vast amount of data across many scientific disciplines. Organizing these data in a meaningful way to support risk assessment has been a significant challenge. To address this and other challenges in modernizing chemical health risk assessment, the Organisation for Economic Cooperation and Development (OECD) formalized the adverse outcome pathway (AOP) framework, an approach to consolidate knowledge into measurable key events (KEs) at various levels of biological organisation causally linked to disease based on the weight of scientific evidence (http://oe.cd/aops). Currently, AOPs have been considered predominantly in chemical safety but are relevant to radiation. In this context, the Nuclear Energy Agency's (NEA's) High-Level Group on Low Dose Research (HLG-LDR) is working to improve research co-ordination, including radiological research with chemical research, identify synergies between the fields and to avoid duplication of efforts and resource investments. To this end, a virtual workshop was held on 7 and 8 October 2020 with experts from the OECD AOP Programme together with the radiation and chemical research/regulation communities. The workshop was a coordinated effort of Health Canada, the Electric Power Research Institute (EPRI), and the Nuclear Energy Agency (NEA). The AOP approach was discussed including key issues to fully embrace its value and catalyze implementation in areas of radiation risk assessment. Conclusions: A joint chemical and radiological expert group was proposed as a means to encourage cooperation between risk assessors and an initial vision was discussed on a path forward. A global survey was suggested as a way to identify priority health outcomes of regulatory interest for AOP development. Multidisciplinary teams are needed to address the challenge of producing the appropriate data for risk assessments. Data management and machine learning tools were highlighted as a way to progress from weight of evidence to computational causal inference.

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In vitro exposure of human lens epithelial cells to X-rays at varied dose-rates leads to protein-level changes relevant to cataractogenesis

Cited by 4 publications

References 40 publications

LncRNA NORAD defects deteriorate the formation of age-related macular degeneration

LncRNA NORAD defects deteriorate the formation of age-related macular degeneration

Introduction to the Second Bill Morgan Memorial Special Issue: an update on low dose biology, epidemiology, its integration and implications for radiation protection

Bringing together scientific disciplines for collaborative undertakings: a vision for advancing the adverse outcome pathway framework

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