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Long non-coding and circular RNA expression profiles in human aortic vascular smooth muscle cells (HAVSMCs)

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE77280 | GEO | 2016/01/28

SECONDARY ACCESSION(S): PRJNA309944

REPOSITORIES: GEO

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The long non-coding RNA(lncRNA) expression profiles in human aortic vascular smooth muscle cells (HAVSMCs)

Project description:To explore the potential involvement of lncRNAs in the vascular smooth muscle cell (VSMC) proliferation, we conducted lncRNA profiling in three pairs of proliferative HAVSMCs and quiescent HAVSMCs by microarray. Our results showed that lncRNAs were aberrantly expressed in proliferative HAVSMCs compared with quiescent HAVSMCs, and provided potential targets for novel insights into VSMC proliferation or vascular remodeling diseases.

2016-01-28 | GSE77279 | GEO

Long non-coding and circular RNA expression profiles in human aortic vascular smooth muscle cells (HAVSMCs)

Project description:Long non-coding and circular RNA expression profiles in human aortic vascular smooth muscle cells (HAVSMCs)

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Protein interaction partners of long non-coding RNA NUDT6 in human aortic smooth muscle cells

Project description:The long non-coding RNA NUDT6 was found to be deregulated in abdominal aortic aneurysm (AAA) with higher expression in diseased human tissue specimens versus control aortic tissue. Apart from the already well-studied DNA: RNA interaction as a natural antisense transcript to Fibroblast Growth Factor 2 (FGF2), we were interested in identifying protein interaction partners to unravel further involvement in the pathogenesis and progression of abdominal aortic aneurysm. Therefore, we performed a RNA pulldown experiment using biotinylated NUDT6 and control RNA in human aortic smooth muscle cell lysate to identify further interaction partners.

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The circular RNA (circRNA) expression profiles in human aortic vascular smooth muscle cells (HAVSMCs)

Project description:To explore the potential involvement of circRNAs in the vascular smooth muscle cell (VSMC) proliferation, we conducted circRNA profiling in three pairs of proliferative HAVSMCs and quiescent HAVSMCs by microarray. Our results showed that circRNAs were aberrantly expressed in proliferative HAVSMCs compared with quiescent HAVSMCs, and provided potential targets for novel insights into VSMC proliferation or vascular remodeling diseases.

2016-01-28 | GSE77278 | GEO

Role of NEIL3 in aortic Vascular Smooth Muscle cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-03-15 | GSE140791 | GEO

Novel Transcript Discovery Expands the Repertoire of Pathologically-Associated, Long Non-Coding RNAs in Vascular Smooth Muscle Cells.

Project description:Vascular smooth muscle cells (VSMCs) provide vital contractile force within blood vessel walls, yet can also propagate cardiovascular pathologies through proliferative and pro-inflammatory activities. Such phenotypes are driven, in part, by the diverse effects of long non-coding RNAs (lncRNAs) on gene expression. However, lncRNA characterisation in VSMCs in pathological states is hampered by incomplete lncRNA representation in reference annotation. We aimed to improve lncRNA representation in such contexts by assembling non-reference transcripts in RNA sequencing datasets describing VSMCs stimulated in vitro with cytokines, growth factors, or mechanical stress, as well as those isolated from atherosclerotic plaques. All transcripts were then subjected to a rigorous lncRNA prediction pipeline. We substantially improved coverage of lncRNAs responding to pro-mitogenic stimuli, with non-reference lncRNAs contributing 21-32% for each dataset. We also demonstrate non-reference lncRNAs were biased towards enriched expression within VSMCs, and transcription from enhancer sites, suggesting particular relevance to VSMC processes, and the regulation of neighbouring protein-coding genes. Both VSMC-enriched and enhancer-transcribed lncRNAs were large components of lncRNAs responding to pathological stimuli, yet without novel transcript discovery 33-46% of these lncRNAs would remain hidden. Our comprehensive VSMC lncRNA repertoire allows proper prioritisation of candidates for characterisation and exemplifies a strategy to broaden our knowledge of lncRNA across a range of disease states.

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Silencing of long non-coding RNA Sox2ot inhibits oxidative stress and inflammation of vascular smooth muscle cells in abdominal aortic aneurysm via microRNA-145-mediated Egr1 inhibition.

Project description:Long non-coding RNAs (lncRNAs) have been largely reported to contribute to the development and progression of abdominal aortic aneurysm (AAA), a common vascular degenerative disease. The present study was set out with the aim to investigate the possible role of lncRNA Sox2ot in the development of AAA. In this study, we found that lncRNA Sox2ot and early growth response factor-1 (Egr1) were highly expressed, while microRNA (miR)-145 was poorly expressed in Ang II-induced AAA mice and oxidative stress-provoked vascular smooth muscle cell (VSMC) model. Egr1 was a potential target gene of miR-145, and lncRNA Sox2ot could competitively bind to miR-145 to upregulate Egr1 expression. Overexpression of miR-145-5p was found to attenuate oxidative stress and inflammation by inhibiting Egr1 both in vivo and in vitro, which was counteracted by lncRNA Sox2ot. Taken together, the present study provides evidence that downregulation of lncRNA Sox2ot suppressed the expression of Egr1 through regulating miR-145, thus inhibiting the development of AAA, highlighting a theoretical basis for AAA treatment.

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Characterization of Circular RNAs in Vascular Smooth Muscle Cells with Vascular Calcification.

Project description:Circular RNAs (circRNAs) are generally formed by back splicing and are expressed in various cells. Vascular calcification (VC), a common complication of chronic kidney disease (CKD), is often associated with cardiovascular disease. The relationship between circRNAs and VC has not yet been studied. Inorganic phosphate (Pi) was used to treat rat vascular smooth muscle cells to induce VC. circRNAs were identified by analyzing RNA sequencing (RNA-seq) data, and their expression change during VC was validated. The selected circRNAs, including circSamd4a, circSmoc1-1, circMettl9, and circUxs1, were resistant to RNase R digestion and mostly localized in the cytoplasm. While silencing circSamd4a promoted VC, overexpressing it reduced VC in calcium assay and Alizarin red S (ARS) staining. In addition, microRNA (miRNA) microarray, luciferase reporter assay, and calcium assay suggested that circSamd4a could act as a miRNA suppressor. Our data show that circSamd4a has an anti-calcification role by functioning as a miRNA sponge. Moreover, mRNAs that can interact with miRNAs were predicted from RNA-seq and bioinformatics analysis, and the circSamd4a-miRNA-mRNA axis involved in VC was verified by luciferase reporter assay and calcium assay. Since circSamd4a is conserved in humans, it can serve as a novel therapeutic target in resolving VC.

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Angiotensin II-induced long non-coding RNA Alivec regulates chondrogenesis in vascular smooth muscle cells

Project description:Alivec is a novel lncRNA found to be upregulated by Ang II stimulation in rat vascular smooth muscle cells (RVSMCs). The regulatory mechanisms of rat Alivec have not been reported so far. We used microarrays to investigate Alivec-mediated global gene expression and identified distinct classes of up- and down-regulated genes.

2021-10-27 | GSE183857 | GEO

Epigenetic control of vascular smooth muscle cells in Marfan and non-Marfan thoracic aortic aneurysms.

Project description:AIMS: Human thoracic aortic aneurysms (TAAs) are characterized by extracellular matrix breakdown associated with progressive smooth muscle cell (SMC) rarefaction. These features are present in all types of TAA: monogenic forms [mainly Marfan syndrome (MFS)], forms associated with bicuspid aortic valve (BAV), and degenerative forms. Initially described in a mouse model of MFS, the transforming growth factor-?1 (TGF-?1)/Smad2 signalling pathway is now assumed to play a role in TAA of various aetiologies. However, the relation between the aetiological diversity and the common cell phenotype with respect to TGF-? signalling remains unexplained. METHODS AND RESULTS: This study was performed on human aortic samples, including TAA [MFS, n = 14; BAV, n = 15; and degenerative, n = 19] and normal aortas (n = 10) from which tissue extracts and human SMCs and fibroblasts were obtained. We show that all types of TAA share a complex dysregulation of Smad2 signalling, independent of TGF-?1 in TAA-derived SMCs (pharmacological study, qPCR). The Smad2 dysregulation is characterized by an SMC-specific, heritable activation and overexpression of Smad2, compared with normal aortas. The cell specificity and heritability of this overexpression strongly suggest the implication of epigenetic control of Smad2 expression. By chromatin immunoprecipitation, we demonstrate that the increases in H3K9/14 acetylation and H3K4 methylation are involved in Smad2 overexpression in TAA, in a cell-specific and transcription start site-specific manner. CONCLUSION: Our results demonstrate the heritability, the cell specificity, and the independence with regard to TGF-?1 and genetic backgrounds of the Smad2 dysregulation in human thoracic aneurysms and the involvement of epigenetic mechanisms regulating histone marks in this process.

| S-EPMC3020128 | biostudies-literature

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