Basic Information
Regular Relationship :
Phenotype/DiseaseSpecieDiabetic Retinopathy
CeRNA1SNHG16[LncRNA]
miRNAmiR-195[miRNA]
CeRNA2mfn2[mRNA]
Tissue/Cell lineretinal microvascular endothelial cells
SpecieHomo sapiens (human)
CitationCurr Pharm Des. 2021 Feb 2. doi: 10.2174/1381612827666210202141541.
Reference title
Decreased lncRNA SNHG16 Accelerates Oxidative Stress Induced Pathological Angiogenesis in Human Retinal Microvascular Endothelial Cells by Regulating miR-195/mfn2 Axis.
Experimental verification
RIP assay;Luciferase reporter assay;
Functional description
BACKGROUND: This study was performed to identify the alterations of Long non-coding RNAs (lncRNAs) induced by oxidative stress and investigate the functional roles of SNHG16 in the pathological angiogenesis by human retinal microvascular endothelial cells (HMRECs). METHODS: The expression profiles of lncRNAs and mRNAs induced by oxidative stress were identified by RNA-Seq, and the dysregulation of 16 lncRNAs including SNHG16 were verified in H2O2-treated human umbilical vein endothelial cells (HUVECs). Luciferase reporter assay and RIP analysis were used to investigate the binding relationship of SNHG16 to miR-195. RESULTS: We confirmed that over-expression of SNGH16 attenuated H2O2-induced angiogenesis by HMRECs. In addition, SNHG16 was significantly decreased whereas miR-195, a predictive target of SNHG16, was upregulated in H2O2, HG, and AGE-treated HMRECs. The binding relationship of SNHG16 to miR-195 was subsequently verified by luciferase reporter assay and RIP analysis. SNHG16 cotransfection abolished miR-195-mediated repression on mitofusin 2 (mfn2) protein level and counteracted the inductive effect of miR-195 on angiogenesis by HMRECs. CONCLUSION: These results indicated that decreased SNHG16 accelerates oxidative stress induced pathological angiogenesis in HMRECs by regulating miR-195/mfn2 axis, providing a potential target for diabetic retinopathy (DR) therapy.
Annotations
External Annotation for SNHG16 |
|
|---|---|
 |
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. |
