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Tytuł:
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lncRNA AABR07005593.1 potentiates PM 2.5 -induced interleukin-6 expression by targeting MCCC1.
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Autorzy:
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Liao F; 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.
Tan Y; 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.
Wang Y; 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.
Zhou C; School of Public Health and Management, YouJiang Medical University for Nationalities, Baise 533000, China.
Wang Q; School of Public Health, Guangxi Medical University, Nanning 530021, China.
Li J; School of Public Health, Guangxi Medical University, Nanning 530021, China.
He L; 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.
Peng X; 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: .
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Źródło:
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Ecotoxicology and environmental safety [Ecotoxicol Environ Saf] 2021 Dec 15; Vol. 226, pp. 112834. Date of Electronic Publication: 2021 Oct 04.
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Typ publikacji:
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Journal Article
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Język:
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English
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Imprint Name(s):
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Original Publication: Amsterdam, Netherlands : Elsevier
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MeSH Terms:
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RNA, Long Noncoding*/genetics
Animals ; Female ; Interleukin-6/genetics ; Male ; NF-kappa B/genetics ; Particulate Matter/toxicity ; Rats ; Rats, Sprague-Dawley
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Contributed Indexing:
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Keywords: PM(2.5); Respiratory inflammation; lncRNA AABR07005593.1
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Substance Nomenclature:
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0 (Interleukin-6)
0 (NF-kappa B)
0 (Particulate Matter)
0 (RNA, Long Noncoding)
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Entry Date(s):
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Date Created: 20211007 Date Completed: 20211020 Latest Revision: 20211020
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Update Code:
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20240104
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DOI:
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10.1016/j.ecoenv.2021.112834
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PMID:
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34619471
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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.
(Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)
