About: MiR-802 alleviates lipopolysaccharide-induced acute lung injury by targeting Peli2

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About: MiR-802 alleviates lipopolysaccharide-induced acute lung injury by targeting Peli2 Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	MiR-802 alleviates lipopolysaccharide-induced acute lung injury by targeting Peli2
Creator	Wang, Jinmei Chang, Yuanmin Jia, Dan Jiang, Lijuan Li, Wenmei You, Qinghai
source	PMC
abstract	INTRODUCTION: Acute respiratory distress syndrome (ARDS) is a life-threatening medical condition. It is characterized by serious lung inflammation or injury. Characterizing novel miRNAs implicated in ARDS pathogenesis may provide new therapeutic strategy for managing ARDS. METHODS: We employed LPS-induced lung injury model to profile miRNAs associated with ARDS. We isolated one miRNA candidate and characterized its role in lipopolysaccharide (LPS)-induced proinflammatory cytokine production in lung macrophages. We further evaluated its functional role in ARDS model by assessing histological change, neutrophil activation, tissue permeability and tumor necrosis factor alpha (TNFα) production. We also characterized its downstream target using luciferase assay, Western blotting, enzyme-linked immunosorbent assay and cell inflammation assay. RESULTS: Microarray profiling revealed miR-802 was significantly downregulated in ARDS mouse model. LPS-induced miR-802 downregulation was confirmed in lung macrophages. Overexpression of miR-802 significantly suppressed LPS-induced inflammatory cytokine production in vitro and alleviates LPS-induced acute lung injury in vivo. Peli2 was identified as a downstream target of miR-802 and found upregulated in ARDS model. Overexpressing Peli2 abolished the antagonizing effect of miR-802 on LPS-mediated inflammatory response. CONCLUSION: MiR-802 carried a protective role against LPS-induced acute lung injury by downregulating Peli2. MiR-802/Peli2 axis may act as intervening targets to manage ARDS.
has issue date	2019-11-06(xsd:dateTime)
bibo:doi	10.1007/s00011-019-01295-z
bibo:pmid	31696241
has license	no-cc
sha1sum (hex)	852ff0ea02f856f63697e67b8a5f567430e20b34
schema:url	https://doi.org/10.1007/s00011-019-01295-z
resource representing a document's title	MiR-802 alleviates lipopolysaccharide-induced acute lung injury by targeting Peli2
has PubMed Central identifier	PMC7223969
has PubMed identifier	31696241
schema:publication	Inflamm Res
resource representing a document's body	covid:852ff0ea02f856f63697e67b8a5f567430e20b34#body_text
is schema:about of	named entity 'tumor necrosis factor alpha' named entity 'lung inflammation' named entity 'acute lung injury' named entity 'profiling' named entity 'ARDS' covid:arg/852ff0ea02f856f63697e67b8a5f567430e20b34 named entity 'Conclusion' named entity 'neutrophil' named entity 'miRNAs' named entity 'downregulated' named entity 'cell' named entity 'strategy' named entity 'Microarray' named entity 'employed' named entity 'lipopolysaccharide' named entity 'tissue' named entity 'lung injury' named entity 'lung' named entity 'assay' named entity 'miRNAs' named entity 'miR' named entity 'miR' named entity 'macrophages' named entity 'Overexpressing' named entity 'miR' named entity 'LPS' named entity 'histological' named entity 'neutrophil' named entity 'miR' named entity 'ARDS' named entity 'proinflammatory cytokine' named entity 'ARDS' named entity 'ARDS' named entity 'acute lung injury' named entity 'Peli2' named entity 'provide' named entity 'Bioinformatics' named entity 'miR-155' named entity 'homogenized' named entity 'LPS' named entity 'miR' named entity 'Peli2' named entity 'ARDS' named entity 'skeletal muscle' named entity 'miR' named entity 'miRNA' named entity 'Roche' named entity 'mRNA' named entity 'ARDS' named entity 'MiRNAs' named entity 'TNFα' named entity 'miR' named entity 'IL-1β' named entity 'downregulated' named entity 'GAPDH' named entity 'morphology' named entity 'miR' named entity 'lung tissue' named entity 'biological role' named entity 'miR' named entity 'protein' named entity 'proinflammatory cytokine secretion' named entity 'miR' named entity 'epithelial-mesenchymal transition' named entity 'monoclonal antibody' named entity 'depression' named entity 'acute lung injury' named entity 'Animal models' named entity 'diffuse alveolar damage' named entity 'downregulated' named entity 'Peli2' named entity 'Reverse Transcription' named entity 'bronchoalveolar lavage fluid' named entity 'downregulated' named entity 'interleukin-1 beta' named entity 'ARDS'

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