Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profiling of miR-128 overexpression in Primary Mouse Vascular Smooth Muscle Cells (VSMCs)

ABSTRACT: MicroRNAs (miRNAs) are small non-coding RNAs that modulate gene expression by negatively regulating translation of target genes. miRNAs involvement in vascular smooth muscle cell (VSMC) biology has been deeply investigated, nevertheless the role of miR-128 in such context has not been yet explored. We aimed to evaluate whether this miR-128 might modulate VSMC phenotype similarly to what was previously observed for other type of contractile cells, such as cardiomyocytes (CM) and skeletal muscle cells. To this end, we compared the expression profiles of miR-128 overexpression in Primary mouse VSMCs and control groups (treated with scrambled miRNA). The expression profiles were defined by Illumina arrays.

ORGANISM(S): Mus musculus

PROVIDER: GSE124764 | GEO | 2020/09/07

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Phenotype modulation of VSMCs on patterned substrate

Project description:Loss of contractility and acquisition of an epithelial phenotype of vascular smooth muscle cells (VSMCs) are key events in proliferative vascular pathologies such as atherosclerosis and post-angioplastic restenosis. There is no proper cell culture system allowing VSMC differentiation so that it is difficult to delineate the molecular mechanism responsible for proliferative vasculopathy. We investigated whether a micro-patterned substrate could restore the contractile phenotype of VSMCs in vitro. To induce and maintain the differentiated VSMC phenotype in vitro, we introduced a micro-patterned groove substrate to modulate the morphology and function of VSMCs.

2013-11-14 | E-MTAB-1888 | biostudies-arrayexpress

Mice VSMCs: Control vs. TNF-α cultured

Project description:Transcriptional profiling of mouse VSMCs comparing control with VSMCs cultured with TNF-α Apoptosis of vascular smooth muscle cells (VSMCs) is a process that regulates vessel remodeling in various cardiovascular diseases. The specific mechanisms that control VSMC apoptosis remain unclear. The present study aimed to investigate whether microRNA-494 (miR-494) is involved in regulating VSMC apoptosis and its underlying mechanisms. Cell death ELISA and terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling assays were used to detect apoptosis of murine VSMCs following stimulation with tumor necrosis factor(TNF-α). The results indicated that TNF-α-upregulated VSMC apoptosis in a dose-dependent manner. Microarray analysis was used to evaluate the expression profile of microRNAs following TNF-α-stimulation in murine VSMCs. The expression of miR-494 was downregulated, whereas B-cell lymphoma 2-like 11 (BCL2L11) protein expression levels were upregulated in VSMCs following treatment with TNF- . Luciferase reporter assays confirmed that BCL2L11 was a direct target of miR-494. Transfection with miR-494 mimics decreased VSMC apoptosis and downregulated BCL2L11 protein levels. Conversely, transfection with miR-494 inhibitors increased cell apoptosis and upregulated BCL2L11 protein levels, suggesting that miR-494 may function as an essential regulator of BCL2L11. The increase in apoptosis caused by miR-494 inhibitors was abolished in cells co-transfected with BCL2L11-targeting small interfering RNA. The findings of the present study revealed that miR-494 inhibited TNF-α-induced VSMC apoptosis by downregulating the expression of BCL2L11.

2019-02-28 | GSE127016 | GEO

Transcription profiling of mouse aorta and vSMCs response to dioxin

Project description:We compared the global gene expression profiles of C57BL/6 mice aortas with the profiles of cultured vascular smooth muscle cells (vSMC) from the same mice, and determined whether gene responses to dioxin exposure in the vSMCs would be predictive of responses in the aorta.

2003-10-29 | E-MEXP-23 | biostudies-arrayexpress

Gene expression profiling of miR-128 overexpression in Primary Mouse Vascular Smooth Muscle Cells (VSMCs)

Project description:Gene expression profiling of miR-128 overexpression in Primary Mouse Vascular Smooth Muscle Cells (VSMCs)

| PRJNA513344 | ENA

Circular non-coding LRP6 is a tissue-enriched circular RNA which regulates smooth muscle cell biology acting as a sponge for miR-145

Project description:Rationale: microRNAs (miRNAs) modulate gene expression by repressing translation of targeted genes. Previous work has established a role for miRNAs in regulating vascular smooth muscle cell (VSMC) activity. Whether circular RNAs (circRNA) are involved in the modulation of miRNA activity in VSMCs is unknown. Objective: We aimed to identify circRNAs interacting with miRNAs enriched in VSMCs and modulating the cells' activity. Methods and Results: RNA sequencing and bioinformatics identified several circRNAs enriched in VSMCs; however, only one, possessing multiple putative binding sites for miR-145, was highly conserved between mouse and man. This circRNA gemmed from alternative splicing of lipoprotein receptor 6 (Lrp6), a gene highly expressed in vessels and implicated in vascular pathologies, and was thus named circ_Lrp6. Its role as a miR-145 sponge was confirmed by determining reciprocal interaction through RNA immunoprecipitation, stimulated emission depletion microscopy, and competitive luciferase assays; functional inhibition of miR-145 was assessed by measuring expression of the target genes ITGβ8, FASCIN, KLF4, Yes1, and Lox. The interaction was preferentially localized to P-bodies, sites of mRNA degradation. Using loss- and gain-of-function approaches, we found that circ_Lrp6 hindered miR-145-mediated regulation of VSMC migration, proliferation, and differentiation. Differential expression of miR-145 and circ_Lrp6 in murine and human vascular diseases suggests that the ratio of circ_Lrp6 bound to miR145 vs. unbound could play a role in vascular pathogenesis. Viral delivery of circ_Lrp6 shRNA prevented intimal hyperplasia in mouse carotids. Conclusions: circ_Lrp6 is an intracellular modulator and a natural sponge for miR-145, counterbalancing the functions of the miRNA in VSMCs.

2018-12-05 | GSE99318 | GEO

miRNA expression profile in rat carotid artery balloon injury model

Project description:The proliferation and remodeling of vascular smooth muscle cells (VSMCs) is an important pathological event in atherosclerosis and restenosis. Here we report that microRNA-132 (miR-132) blocks vascular smooth muscle cells (VSMC) proliferation by inhibiting the expression of LRRFIP1 [leucine-rich repeat (in Flightless 1) interacting protein-1]. MicroRNA microarray revealed that miR-132 was upregulated in the rat carotid artery after catheter injury, which was further confirmed by quantitative real-time RT-PCR. Transfection of an miR-132 mimic significantly inhibited the proliferation of VSMCs, whereas transfection of an miR-132 antagomir increased it. Bioinformatics showed that LRRFIP1 is a target candidate of miR-132. miR-132 down-regulated luciferase activity driven by a vector containing the 3’-untranslated region of Lrrfip1 in a sequence-specific manner. LRRFIP1 induced VSMC proliferation. Immunohistochemical analysis revealed that Lrrfip1 was clearly expressed along with the basal laminar area of smooth muscle, and its expression pattern was disrupted 7 days after arterial injury LRRFIP1 mRNA was decreased 14 days after injury. Delivery of miR-132 to rat carotid artery attenuated neointimal proliferation in carotid artery injury models. Our results suggest that miR-132 is a novel regulator of VSMC proliferation that represses neointimal formation by inhibiting LRRFIP1 expression. Balloon injury was induced in the carotid arteries of male Sprague–Dawley rats weighing approximately 250 g. Total RNA were extracted from the arterial sections after 10 days. MicroRNA profile of the sample was compared with non-injured control.

2013-04-23 | E-GEOD-45433 | biostudies-arrayexpress

Aging aggravates aortic aneurysm and dissection via the miR-1204-MYLK signaling axis

Project description:The mechanism by which aging induces aortic aneurysm and dissection (AAD) remains unclear. A total of 430 subjects were recruited for screening of differentially expressed plasma microRNAs. We found that miR-1204 was significantly increased in both plasma and aorta of elder patients with AAD, and was positively correlated with age. Cell senescence induced the expression of miR-1204 through p53 interaction with plasmacytoma variant translocation 1, and miR-1204 induced vascular smooth muscle cell (VSMC) senescence to form a positive feedback loop. miR-1204 aggravated angiotensin II-induced AAD formation, and inhibition of miR-1204 attenuated β-aminopropionitrile monofumarate-induced AAD formation. Mechanistically, miR-1204 directly targeted myosin light chain kinase (MYLK) to promote VSMCs to acquire senescence-associated secretory phenotype (SASP) and lose their contractile phenotype. Overexpression of MYLK reversed miR-1204-induced VSMC senescence, SASP and contractile phenotype changes, and the decrease of transforming growth factor-β signaling pathway. Our findings suggest aging aggravates AAD via miR-1204-MYLK signaling axis.

2024-04-01 | PXD048658 | Pride

Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration [miRNA-seq]

Project description:To identify the potential microRNAs (miRNAs) involved in the regulation of cardiomyocyte (CM) proliferation during homeostasis and injury, RNA sequencing (RNA-seq) in mouse cardiac ventricles was performed on postnatal day 1, 7, and 28 (P1, P7, and P28). Significant upregulation of MiR-128 was found in P7 hearts as compared to P1. To further specify the effect of miR-128 in the heart, RNA-Seq was performed in control mice (Ctrl) and miR-128 overexpression mice (miR-128OE) on P7. These data provide novel insights into the mechanisms by which adult CMs exit the cell cycle arrest and is fundamental for therapeutic manipulation to stimulate endogenous CM proliferate in cardiac regeneration.

2018-01-02 | GSE107679 | GEO

Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration [RNA-seq]

2018-01-02 | GSE107678 | GEO

MT1-MMP (MMP14)-dependent gene expression in APOE-null vascular smooth muscle cells (VSMCs)

Project description:VSMC-specific MT1-MMP gene targeting in APOE-null mice promotes atherosclerosis and iliac artery aneurysm formation. To determine the MT1-MMP-dependent regulation of VSMC function, whole-genome transcriptomes of wild-type and MT1-MMP-null APOE-null VSMCs were determined. We used microarray-based transcriptome analysis to detect MT1-MMP-dependent regulation of VSMC function under atherogenic conditions.

2017-08-01 | GSE100661 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data