Basic Information
Regular Relationship :
Phenotype/DiseaseSpecieDiabetic Nephropathy
CeRNA1NORAD[LncRNA]
miRNAmiR-485[miRNA]
CeRNA2NRF1[mRNA]
Tissue/Cell lineHuman Mesangial Cells
SpecieHomo sapiens (human)
CitationExp Ther Med. 2021 Aug;22(2):874. doi: 10.3892/etm.2021.10306. Epub 2021 Jun 14.
Reference title
Knockdown of lncRNA NORAD inhibits the proliferation, inflammation and fibrosis of human mesangial cells under high-glucose conditions by regulating the miR-485/NRF1 axis.
Experimental verification
Dual-luciferase reporter assay;ELISA;MTT assay;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;MTT assay;
Functional description
Long non-coding RNAs (lncRNAs) serve major roles in diabetic nephropathy (DN). The present study investigated the regulatory mechanism of lncRNA non-coding RNA activated by DNA damage (NORAD) on DN in vitro. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of lncRNA NORAD, microRNA-485 (miR-485) and nuclear respiratory factor 1 (NRF1) in the tissues of patients with DN and high-glucose (HG)-induced human mesangial cells (HMCs). The viability of HMCs was determined using an MTT assay. The levels of inflammatory [tumour necrosis factor (TNF)-a, interleukin (IL)-1b and IL-6] and fibrotic [type IV collagen (Col. IV), fibronectin (FN) and plasminogen activator inhibitor 1 (PAI-1)] factors in HMCs were measured by ELISA. The interactions between miR-485 and NORAD/NRF1 were predicted using StarBase and miRDB softwares and confirmed by a dual-luciferase reporter assay. Western blot analysis was utilized to measure NRF1 protein levels. lncRNA NORAD was highly expressed in tissues and HG-induced HMCs. NORAD knockdown suppressed cell viability in HG-induced HMCs. The levels of the inflammatory and fibrotic factors in HG-induced HMCs were inhibited by NORAD knockdown. miR-485 was the direct target of NORAD. NORAD reversed the inhibitory effects of miR-485 on HG-induced HMCs. Furthermore, NRF1 was the target gene of miR-485. Downregulation of miR-485 and upregulation of NRF1 reversed the inhibitory effects of NORAD knockdown on HG-induced HMCs. NORAD knockdown inhibited HG-induced HMC proliferation, inflammation and fibrosis by regulating miR-485/NRF1, providing a possible therapeutic strategy for DN.
Annotations
External Annotation for NORAD |
|
|---|---|
 |
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. |
