Details

Autor(en) / Beteiligte

• Li, Bin
• Huang, Nannan
• Wei, Shengnan
• Xv, Jie
• Meng, Qingtao
• Aschner, Michael
• Li, Xiaobo
• Chen, Rui

Titel

lncRNA TUG1 as a ceRNA promotes PM exposure-induced airway hyper-reactivity

Ist Teil von

• Journal of hazardous materials, 2021-08, Vol.416, p.125878-125878, Article 125878

Ort / Verlag

Elsevier B.V

Erscheinungsjahr

2021

Quelle

Alma/SFX Local Collection

Beschreibungen/Notizen

• With the increased appreciation for the significance of noncoding RNAs (ncRNAs), the present research aimed to determine the role of competing endogenous RNA (ceRNA) in the process of particulate matter (PM) exposure-induced pulmonary damage. Alterations in messenger RNA (RNA), microRNA and long non-coding RNA (lncRNA) profiles of human bronchial epithelial (HBE) cells treated with PM were analyzed by microarray assays. Next, we identified that lncRNA taurine upregulated gene 1 (TUG1) acted as a competing endogenous RNA for microRNA-222-3p (miR-222-3p) and subsequently attenuated the inhibitory effect of miR-222-3p on CUGBP elav-like family member 1 (CELF1). The binding potency among ceRNAs was verified by RNA immunoprecipitation (RIP) assay and dual-luciferase reporter assay. Knockdown of TUG1 attenuated HBE cell apoptosis and cell cycle arrest by downregulation of CELF1 and protein 53 (p53). Further, we confirmed that Tug1/mir-222-3p/CELF1/p53 network aggravated PM-induced airway hyper-reactivity (AHR) in mice. In summary, our novel findings revealed that TUG1 triggered dysfunction of pulmonary cells followed by PM exposure by serving as a sponge for miR-222-3p and thereby upregulating the expression of CELF1and p53. [Display omitted] •Inhaled particulate matter (PM) induces alterations in RNAs.•The TUG1/miR-222-3p/CELF1/p53 network mediates apoptosis and cell cycle arrest upon PM exposure.•Mice treated with antisense oligonucleotides for Tug1 are protected from PM-induced airway hyper-reactivity.