Arsenite Increases Linc-ROR in Human Bronchial Epithelial Cells that Can Be Inhibited by Antioxidant Factors
- PDF / 1,657,684 Bytes
- 11 Pages / 595.276 x 790.866 pts Page_size
- 69 Downloads / 174 Views
Arsenite Increases Linc-ROR in Human Bronchial Epithelial Cells that Can Be Inhibited by Antioxidant Factors Xinyang Li 1 & Chao Zuo 1 & Donglei Sun 1 & Tianhe Zhao 1 & Zunzhen Zhang 1 Received: 16 December 2019 / Accepted: 30 January 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Oxidative stress is the main mechanism of arsenite toxicity. Long intergenic non-coding RNA regulator of reprogramming is a newly found stress-response long non-coding RNA that is activated in various stress conditions. However, whether long intergenic non-coding RNA, regulator of reprogramming (linc-ROR) is involved in arsenite-induced oxidative stress has not been explored. In this study, we found that arsenite dose responsively increased the expression of linc-ROR in human bronchial epithelial (HBE) cells, along with elevated oxidative stress demonstrated by increased intracellular reactive oxygen species (ROS) and DNA damage, as well as decreased antioxidant glutathione and superoxide dismutase. We further found that the pre-treatment with N-acetylcysteine, a widely used ROS scavenger, and the over-expression of antioxidant NRF2 protein, both significantly reduced arsenite-induced oxidative stress in arsenite-treated HBE cells, and the linc-ROR over-expression was also inhibited, suggesting that oxidative stress is a key factor for the increase of linc-ROR in arsenite-treated HBE cells. Moreover, our results of bio-informatic analysis showed that arsenite-induced oxidative stress might modulate linc-ROR expression via 3 genes and the up-regulated linc-ROR in arsenite-induced oxidative stress may get involved in cellular processes such as cellular stress response, RNA metabolism, and DNA repair. Collectively, our study demonstrates that oxidative stress plays the key role in arsenite-induced over-expression of linc-ROR, and linc-ROR may be a new clue for exploring the mechanism of arsenite toxicity. Keywords Linc-ROR . Arsenite . Oxidative stress . Antioxidants
Introduction Long non-coding RNAs (lncRNAs) are a new class of transcripts longer than 200 nucleotides and play roles in cell development, differentiation, and homeostasis [1, 2]. The aberrant expression of lncRNAs is closely related to pathological process and human diseases such as inflammation, metabolic disorder, and tumorigenesis [3–5]. It has been reported that stress conditions, including oxidative stress, hypoxic stress, and chemotherapy, can lead to up-regulation of many lncRNAs [6–9]. Among these lncRNAs, long intergenic Electronic supplementary material The online version of this article (https://doi.org/10.1007/s12011-020-02065-3) contains supplementary material, which is available to authorized users. * Zunzhen Zhang [email protected]; [email protected] 1
West China School of Public Health and West China Fourth Hospital, Sichuan University, No. 16, Section 3, Renmin Nanlu, 610041 Chengdu, People’s Republic of China
non-coding RNA ROR (regulator of reprogramming, lincROR), a lncRNA initially found to regulate the conversion
Data Loading...
