1. Academic Validation
  2. PM2.5-inducible long non-coding RNA (NONHSAT247851.1) is a positive regulator of inflammation through its interaction with raf-1 in HUVECs

PM2.5-inducible long non-coding RNA (NONHSAT247851.1) is a positive regulator of inflammation through its interaction with raf-1 in HUVECs

  • Ecotoxicol Environ Saf. 2020 Jun 15;196:110476. doi: 10.1016/j.ecoenv.2020.110476.
CaiLan Zhou 1 Yi Tan 2 YuYu Wang 2 FangPing Liao 1 QiuLing Wang 1 JingLin Li 1 SuJuan Peng 3 XiaoWu Peng 4 YunFeng Zou 5
Affiliations

Affiliations

  • 1 School of Public Health, Guangxi Medical University, Nanning, 530021, China.
  • 2 State Environmental Protection Key Laboratory of Environmental Pollution Health Risk Assessment, South China Institute of Environmental Sciences, Ministry of Ecology and Environment, Guangzhou, 510535, China.
  • 3 School of Public Health, Wuhan University of Science and Technology, Wuhan, 430081, China.
  • 4 School of Public Health, Guangxi Medical University, Nanning, 530021, China; State Environmental Protection Key Laboratory of Environmental Pollution Health Risk Assessment, South China Institute of Environmental Sciences, Ministry of Ecology and Environment, Guangzhou, 510535, China. Electronic address: pengxiaowu@scies.org.
  • 5 School of Public Health, Guangxi Medical University, Nanning, 530021, China. Electronic address: zouyunfeng@gxmu.edu.cn.
Abstract

Several studies have demonstrated that PM2.5 inhalation is associated with an increased risk of cerebrovascular disease (CVD), in which inflammation plays an important role. The mechanisms of this disease are not fully understood to date. Long non-coding RNAs (lncRNAs) are involved in many pathophysiological processes, such as immune responses; however, their functions associated with inflammation are largely unexplored. High-throughput Sequencing assay and obtained numerous lncRNAs that altered the expression in response to PM2.5 treatment in HUVECs. NONHSAT247851.1 was also identified, which was significantly up-regulated to control the expression of immune response genes. Mechanistically, the results indicated that NONHSAT247851.1 knockdown reduced the expression of IL1β. In study, we investigated NONHSAT247851.1 as a promoter in regulating immune response genes via binding with raf-1 to regulate the phosphorylation level of p65 protein in HUVECs. The data collected suggests that NONHSAT247851.1 regulates inflammation via interaction with raf-1 to control the inflammatory expression in PM2.5 exposure.

Keywords

Cerebrovascular disease; Inflammation; NONHSAT247851.1; PM(2.5).

Figures
Products