lncRNA AABR07005593.1 potentiates PM2.5-induced interleukin-6 expression by targeting MCCC1

FangPing Liao; Yi Tan; YuYu Wang; CaiLan Zhou; QiuLing Wang; JingLin Li; LiMei He; XiaoWu Peng

doi:10.1016/j.ecoenv.2021.112834

lncRNA AABR07005593.1 potentiates PM_2.5-induced interleukin-6 expression by targeting MCCC1

Ecotoxicol Environ Saf. 2021 Dec 15:226:112834. doi: 10.1016/j.ecoenv.2021.112834. Epub 2021 Oct 4.

Authors

FangPing Liao¹, Yi Tan², YuYu Wang², CaiLan Zhou³, QiuLing Wang⁴, JingLin Li⁴, LiMei He², XiaoWu Peng⁵

Affiliations

¹ 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; 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 and Management, YouJiang Medical University for Nationalities, Baise 533000, China.
⁴ School of Public Health, Guangxi Medical University, Nanning 530021, China.
⁵ 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.

PMID: 34619471
DOI: 10.1016/j.ecoenv.2021.112834

Abstract

Background: Fine particle pollution, specifically pollution by fine particulate matter (PM_2.5), remains a significant concern in developing countries and plays an important role in the development and progression of respiratory diseases. Increasing evidences have demonstrated that long non-coding RNAs (lncRNAs) may act as vital molecules by binding to specific RNA-binding protein (RBP); however, their relationship with PM_2.5 pollution is largely unexplored.

Objective: We investigated the association between lncRNA and respiratory system inflammation caused by PM_2.5.

Methods: PM_2.5 components were detected by gas chromatography-mass spectrometry (GC-MS), inductively coupled plasma-mass spectrometry (ICP-MS), and ionic chromatography. We established an inflammation model of PM_2.5-induced toxicity in vivo (male and female SD rats, 0, 25, 50 and 100 mg/k PM_2.5, 1, 7 and 14 days, single non-invasive tracheal instillation) and in vitro (rat alveolar macrophage cell line (NR8383), 0, 50, 100, 200, 400 μM PM_2.5 for 24, 48, and 72 h). lncRNA high-throughput sequencing (lncRNA-seq) was used to investigate lncRNA profiles in PM_2.5-treated NR8383 cells, and RNA interference (RNAi) was applied to explore the function of the target lncRNA. The mechanisms associated with specific lncRNAs were explored using comprehensive identification of RNA-binding proteins by mass spectrometry (ChIRP-MS) and western blot.

Results: PM_2.5-treated NR8383 cells and SD rats exhibited respiratory inflammation. lncRNA AABR07005593.1 was a pro-inflammatory factor that regulated IL-6 levels. Mechanistically, ChIRP-MS and western blot analyses revealed that highly expressed lncRNA AABR07005593.1 interacted with MCCC1 to involve in the activation of NF-κB pathway, and ultimately promoted the expression of IL-6.

Conclusion: This study demonstrated that PM_2.5 induced inflammation in vivo and in vitro. Furthermore, lncRNA AABR07005593.1 bound to MCCC1 to potentiated IL-6 expression. Therefore, lncRNA AABR07005593.1 may act as a potential biomarker for PM_2.5 inflammation.

Keywords: PM(2.5); Respiratory inflammation; lncRNA AABR07005593.1.

MeSH terms

Animals
Female
Interleukin-6 / genetics
Male
NF-kappa B / genetics
Particulate Matter / toxicity
RNA, Long Noncoding* / genetics
Rats
Rats, Sprague-Dawley

Substances

Interleukin-6
NF-kappa B
Particulate Matter
RNA, Long Noncoding