Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mir-483 regulates the senescence of human adipose-derived mesenchymal stem cells through IGF1

ABSTRACT: Mir-483 regulates the senescence of human adipose-derived mesenchymal stem cells through IGF1

PROVIDER: PRJNA577678 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10280160_1.fastq.gz	Fastqsanger.gz
	SRR10280160_2.fastq.gz	Fastqsanger.gz
	SRR10280161_1.fastq.gz	Fastqsanger.gz
	SRR10280161_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

MiR-483 induces senescence of human adipose-derived mesenchymal stem cells through <i>IGF1</i> inhibition.

Project description:Human adipose-derived mesenchymal stem cells (hADSCs) are an ideal source of seed cells for regenerative applications and tissue engineering. However, long-term in vitro culture of hADSCs reduces their quantity and quality, which lessens their value in research and clinical applications. The molecular mechanisms underlying this biological process are poorly defined. Recently identified microRNAs (miRNAs) have emerged as critical modulators of cellular senescence. In this study, we examined the changes in hADSCs undergoing senescence. Significant miR-483-3p upregulation was noted during in vitro passaging of hADSCs, which correlated with the adipogenic differentiation and cellular senescence. Knockdown of miR-483-3p retarded the adipogenic differentiation potential of hADSCs and reduced cellular senescence. Dual-luciferase reporter assays identified insulin-like growth factor-1 (IGF1) as the target gene of miR-483-3p. IGF1 inhibition confirmed its inhibitory effects on replicative senescence in hADSCs. In conclusion, our study revealed essential regulatory roles of miR-483-3p in the adipogenesis and aging of hADSCs mediated by targeting IGF1.

| S-EPMC7467354 | biostudies-literature

Mir-483 regulates the senescence of human adipose-derived mesenchymal stem cells through IGF1

Project description:We performed small-RNA sequencing using adipogenic differentiation samples from day 0 (undifferentiated) and day 14.

2020-09-21 | GSE138879 | GEO

miR-483 to 8OH-G miR-483 transversion changes mRNA targetomes in Ecs

Project description:To explore the transcriptional changes in endothelial cells (ECs) caused by the 8OH-G miR-483 transversion, we overexpressed miR-483 or 8OH-G miR-483 in ECs and profiled transcriptomes by RNA-seq We then performed gene expression profiling analysis using data obtained from RNA-seq.

2023-03-07 | GSE226665 | GEO

miR-483 to 8OH-G miR-483 transversion changes mRNA targetomes in Ecs

Project description:miR-483 to 8OH-G miR-483 transversion changes mRNA targetomes in Ecs

| PRJNA941193 | ENA

Transcriptome data of miR-483 overexpression in human pulmonary arterial endothelial cells

Project description:MicroRNA-483 (miR-483) regulate endothelial function through inhibition expression of connective tissue growth factor (CTGF). Endothelial dysfunction is involved in the pathogeneis of pulmonary arterial hypertension (PAH). We investigated the role of miR-483 overexpression on human pulmonary arterial endothelial cells (hPAECs) through comparing the transcriptome file of hPAECs transfected with miR-483 -3p and -5p mimic and with control mimic. Gene ontology analysis showed that several PAH-associated signaling pathways were regulated by miR-483, including transforming growth factor-β signaling, Wnt signaling and inflammatory response, cell adhesion, response to hypoxia, apoptotic processes, oxidative reduction processes and negative regulation of cell migration and proliferation.

2020-03-16 | GSE146774 | GEO

Overexpression of miR-483-3p in human keratinocytes

Project description:HaCaT human keratinocytes were transfected with pre-miR-483-3p or pre-miR-NC. RNA samples were harvested 48h post-transfection and mRNA profiles were determined with pan genomic arrays. Two biological replicates were performed for each comparison. Data were normalized using a dye-swap method.

2011-06-29 | GSE19931 | GEO

miR-483 overexpression in human sarcoma cell line MHH-ES-1.

2013-12-31 | GSE50980 | GEO

Identification of genes suppressed by miR-483-5p and miR-551a in a colon cancer cell-line

Project description:miR-483-5p and miR-551a were over-expressed in a colon cancer cell-line LvM3b to identify genes that are down-regulated by the miRNAs over-expression. Total RNA was isolated from miR-483-5p or miR-551a over-expressing LvM3b cells as well as control LvM3b cells.

2015-01-16 | E-GEOD-63041 | biostudies-arrayexpress

Identification of genes suppressed by miR-483-5p and miR-551a in a colon cancer cell-line

Project description:miR-483-5p and miR-551a were over-expressed in a colon cancer cell-line LvM3b to identify genes that are down-regulated by the miRNAs over-expression.

2015-01-16 | GSE63041 | GEO

miR-483 overexpression in human sarcoma cell line MHH-ES-1.

Project description:miRNA abnormalities are increasingly relevent to cancer development, We used microarrays to detail the global programme of gene expression upon miR-483 overexpression in sarcoma cell line MHH-ES-1. MHH-ES-1 cells were transfected with miR-483-5p, -3p or scrambled control mimics and then harvested 48 hours after to isolate total RNAs using Trizol reagent (Invitrogen). Total RNA was converted to cRNA probes using the BioArray High Yield Transcript Labeling Kit (ENZO diagnostics), and hybridized to Affymetrix GeneChip human HG-U133ver2+ 3’-mRNA expression microarray chips using protocol EukGEs2v4 on the GeneChip Fluidic Station.

2013-12-31 | E-GEOD-50980 | biostudies-arrayexpress

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