RGD Reference Report - LncRNA SNHG1 alleviates hypoxia-reoxygenation-induced vascular endothelial cell injury as a competing endogenous RNA through the HIF-1α/VEGF signal pathway. - Rat Genome Database

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LncRNA SNHG1 alleviates hypoxia-reoxygenation-induced vascular endothelial cell injury as a competing endogenous RNA through the HIF-1α/VEGF signal pathway.

Authors: Liang, Shuangchao  Ren, Kai  Li, Buying  Li, Fangkuan  Liang, Zhuowen  Hu, Jiqiong  Xu, Bei  Zhang, Andong 
Citation: Liang S, etal., Mol Cell Biochem. 2020 Feb;465(1-2):1-11. doi: 10.1007/s11010-019-03662-0. Epub 2019 Dec 2.
RGD ID: 329337374
Pubmed: PMID:31792649   (View Abstract at PubMed)
DOI: DOI:10.1007/s11010-019-03662-0   (Journal Full-text)

Long noncoding ribonucleic acids (lncRNAs) are critical regulators in various biological processes. In the present study, we aimed to explore whether miR140-3p was involved in the underlying molecular mechanisms of small nucleolar RNA host gene 1 (SNHG1) in myocardial ischemia/reperfusion (I/R) injury. A mouse model of I/R injury and hypoxia-reoxygenation (H/R)-stimulated human umbilical vein endothelial cells (HUVECs) was used in this study. Cell proliferation was detected by MTT. The mRNA and protein levels of vascular endothelial growth factor (VEGF), VE-cadherin, and MMP2 were detected by RT-PCR and western blot, respectively. The angiogenesis was assessed by tube formation assay. Cell migration was assessed using wound-healing assay. Results showed that SNHG1 expression was increased in the cardiac microvasculature of a mouse model of I/R injury and in H/R-stimulated HUVECs. H/R stimulation significantly reduced cell proliferation, tube formation, and cell migration, but increased expression of VEGF, VE-cadherin, and MMP2. SNHG1 upregulation under H/R increased HUVECs proliferation, tube formation, and cell migration, and upregulated expression of VEGF, VE-cadherin, and MMP2, compared with the H/R group. SNHG1 knockdown exhibited the opposite effect. SNHG1 functioned as a competing endogenous RNA (ceRNA) of miR-140-3p. HIF-1α was identified as a target of miR-140-3p. SNHG1 upregulation enhanced cell proliferation, tube formation, and expression of VEGF, VE-cadherin, and MMP2 through HIF-1α/VEGF signaling. This process could be offset by miR-140-3p mimic or VEGF inhibitor. Our results reveal a novel protective function of SNHG1 that furthers understanding of cardiac I/R injury and provides experimental evidence for future therapy.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
MIR140HumanMyocardial Reperfusion Injury  ISOMir140 (Mus musculus)miRNA:increased expression:heart and endothelial cells (mouse)RGD 
Mir140MouseMyocardial Reperfusion Injury  IEP miRNA:increased expression:heart and endothelial cells (mouse)RGD 
Mir140RatMyocardial Reperfusion Injury  ISOMir140 (Mus musculus)miRNA:increased expression:heart and endothelial cells (mouse)RGD 
Snhg1MouseMyocardial Reperfusion Injury  IEP mRNA:altered expression:heart and endothelial cell (mouse)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Mir140  (microRNA 140)

Genes (Mus musculus)
Mir140  (microRNA 140)
Snhg1  (small nucleolar RNA host gene 1)

Genes (Homo sapiens)
MIR140  (microRNA 140)


Additional Information