1. Academic Validation
  2. Circular RNA 406961 interacts with ILF2 to regulate PM2.5-induced inflammatory responses in human bronchial epithelial cells via activation of STAT3/JNK pathways

Circular RNA 406961 interacts with ILF2 to regulate PM2.5-induced inflammatory responses in human bronchial epithelial cells via activation of STAT3/JNK pathways

  • Environ Int. 2020 Aug;141:105755. doi: 10.1016/j.envint.2020.105755.
Yangyang Jia 1 Xin Li 1 Aruo Nan 2 Nan Zhang 2 Lijian Chen 2 Hanyu Zhou 2 Han Zhang 2 Miaoyun Qiu 2 Jialu Zhu 2 Yihui Ling 2 Yiguo Jiang 3
Affiliations

Affiliations

  • 1 State Key Laboratory of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510120, China; Institute for Chemical Carcinogenesis, Guangzhou Medical University, Guangzhou 511436, China.
  • 2 Institute for Chemical Carcinogenesis, Guangzhou Medical University, Guangzhou 511436, China.
  • 3 State Key Laboratory of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510120, China; Institute for Chemical Carcinogenesis, Guangzhou Medical University, Guangzhou 511436, China. Electronic address: jiangyiguo@gzhmu.edu.cn.
Abstract

Fine particulate matter (PM2.5) has been verified to augmented the incidence of pneumonia, asthma, pulmonary fibrosis, and other pulmonary diseases. Airway inflammation is the pathological basis of the respiratory system, and understanding the molecular mechanisms responsible for airway inflammation may thus support the diagnosis and treatment of respiratory diseases. In our study, human bronchial epithelial cells (BEAS-2B) were exposed to various concentrations of PM2.5 for 48 h. PM2.5 entered the cells, resulting in increased production of interleukin 6 (IL-6) and interleukin 8 (IL-8) and decreased the expression of circular RNA 406961 (circ_406961). Further, PM2.5 with a concentration of 75 μg/mL was applied to mechanism study. Functional experiments further confirmed that circ_406961 inhibited PM2.5-induced BEAS-2B cell inflammation. RNA pull-down and mass spectrometry showed that circ_406961 interacted with interleukin enhancer-binding factor 2 (ILF2), which could regulate phosphorylation of signal transducer and activator of transcription 3 (STAT3) and mitogen-activated protein kinase 8 (MAPK8, JNK). Our studies showed that circ_406961 inhibited activation of STAT3/JNK pathways via interacting with ILF2 protein, thereby inhibiting the PM2.5-induced inflammatory reaction.

Keywords

Circ_406961; ILF2; Inflammatory reaction; PM(2.5); STAT3/JNK pathways.

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