Detail (Experimental CeRNA)

Home Detail(Experimental CeRNA)

Basic Information

Regular Relationship :


Phenotype/DiseaseSpecie

Acute Lung Injury

CeRNA1

OIP5-AS1[LncRNA]

miRNA

miR-26a-5p[miRNA]

CeRNA2

TLR4[mRNA]


Tissue/Cell line

Ali Mice And Lps-Treated Primary Bronchial/Tracheal Epithelial Cells

Specie

Mus musculus (mouse)

Citation

BMC Pulm Med. 2021 Jul 14;21(1):236. doi: 10.1186/s12890-021-01589-1.


Reference title
Long non-coding RNA OIP5-AS1 aggravates acute lung injury by promoting inflammation and cell apoptosis via regulating the miR-26a-5p/TLR4 axis.
Experimental verification
RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;

Functional description
BACKGROUND: Acute lung injury (ALI) is a pulmonary disorder that leads to acute respiration failure and thereby results in a high mortality worldwide. Increasing studies have indicated that toll-like receptor 4 (TLR4) is a promoter in ALI, and we aimed to explore the underlying upstream mechanism of TLR4 in ALI. METHODS: We used lipopolysaccharide (LPS) to induce an acute inflammatory response in vitro model and a murine mouse model. A wide range of experiments including reverse transcription quantitative polymerase chain reaction, western blot, enzyme linked immunosorbent assay, flow cytometry, hematoxylin-eosin staining, RNA immunoprecipitation, luciferase activity and caspase-3 activity detection assays were conducted to figure out the expression status, specific role and potential upstream mechanism of TLR4 in ALI. RESULT: TLR4 expression was upregulated in ALI mice and LPS-treated primary bronchial/tracheal epithelial cells. Moreover, miR-26a-5p was confirmed to target TLR4 according to results of luciferase reporter assay. In addition, miR-26a-5p overexpression decreased the contents of proinflammatory factors and inhibited cell apoptosis, while upregulation of TLR4 reversed these effects of miR-26a-5p mimics, implying that miR-26a-5p alleviated ALI by regulating TLR4. Afterwards, OPA interacting protein 5 antisense RNA 1 (OIP5-AS1) was identified to bind with miR-26a-5p. Functionally, OIP5-AS1 upregulation promoted the inflammation and miR-26a-5p overexpression counteracted the influence of OIP5-AS1 upregulation on cell inflammatory response and apoptosis. CONCLUSION: OIP5-AS1 promotes ALI by regulating the miR-26a-5p/TLR4 axis in ALI mice and LPS-treated cells, which indicates a promising insight into diagnostics and therapeutics in ALI.

Annotations

External Annotation for OIP5-AS1
LncRNA-associated competing triplets and functions.
Comprehensive experimentally supported associations between lncRNA and human cancer.
Infer genomic variations that disturb lncRNA-associated ceRNA regulation..
Provide and annotate disease or phenotype-associated variants in human long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) or their regulatory elements.
Providing cellular-specific lncRNA-associated ceRNA networks predicted via high-throughput analysis of single-cell genomic data.
Information on all annotated and predicted human genes.
Gene nomenclature, gene families and associated resources (genomic, proteomic, phenotypic information).
Genome browser for vertebrate genomes.
An annotated collection of all publicly available DNA sequences.
A wiki-based platform for community curation of human long non-coding RNAs.
An integrated knowledge database dedicated to non-coding RNAs.
An integrated database of human annotated lncRNA transcripts.
Comprehensive annotations of eukaryotic long non-coding RNAs.
Comprehensive experimentally supported associations between lncRNA and human cancer.
A comprehensive, authoritative compendium of human genes and genetic phenotypes.
The catalogue of somatic mutations in cancer.

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