Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome profiling of cartilage progenitor cells over-expressing miR-138 or miR-181a/b-1 during chondrogenic induction

ABSTRACT: The goal of this study was to investigate the effects of miR-138 or miR-181a/b-1 on regulating chondrogenesis. Gene expression profiles were analyzed in human cartilage progenitor cells (CPCs) over-expressing either miR-138 or miR-181a/b-1 following 7 days of chondrogenic induction in high cell density pellet cultures under hypoxic conditions (5% O2). CPCs were isolated from human osteoarthritic articular cartilage and over-expression of miR-138 or miR-181a/b-1 was achieved via lentiviral transduction of the precursor form of miR-138 or miR-181a/b-1. Control CPCs were transduced with lentivirus expressing a non-silencing (NS) control RNA sequence. Total RNA was harvested at day 7 of chondrogenic induction and subjected to RNA-Seq analysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE262978 | GEO | 2024/11/21

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptome profiling of cartilage progenitor cells over-expressing miR-138 or miR-181a/b-1 during chondrogenic induction

Project description:Transcriptome profiling of cartilage progenitor cells over-expressing miR-138 or miR-181a/b-1 during chondrogenic induction

| PRJNA1095370 | ENA

Transcriptome profiling of de-differentiated chondrocytes over-expressing miR-138 or miR-181ab1 during osteogenic induction

Project description:The goal of this study was to investigate the effects of miR-138 or miR-181ab1 on regulating osteogenesis. Gene expression profiles were analyzed in human de-differentiated chondrocytes (DDCs) over-expressing either miR-138 or miR-181ab1 following day 2 or day 7 of osteogenic induction. DDCs were isolated from human osteoarthritic articular cartilage and over-expression of miR-138 or miR-181ab1 was induced following lentiviral transduction of DDCs over-expressing the precursor form of miR-138 or miR-181ab1. Control DDCs were transduced with lentivirus expressing a non-silencing (NS) control RNA. Total RNA was harvested at day 2 or day 7 following osteogenic induction and subjected to RNA-Seq analysis.

2018-01-12 | GSE109108 | GEO

Project description:Aging is a major risk factors for osteoarthritis (OA), and cartilage of the elder are more sensitive to mechanical loading stress. Recently, cartilage progenitor cells (CPCs) arose much interests due to its important role in maintaining cartilage homeostasis. However, the potential mechanism of increased sensitivity to mechanical stress in CPCs has not been elucidated. The aim of this study was to investigate the potential links between aging and age-related OA through establish CPCs replicative senescence model and fluid flow shear stress (FFSS) stimulated degeneration model. Small RNA and mRNA sequence were conducted to investigate miRNA-related mechanisms in this process. By gain-and-lost strategy we investigated the age-related miRNAs and their impacts on exacerbating the progression of biomechanical stimulated TMJ-OA. miR-708-5p was identified as age-related miRNA in CPCs, and TLR4 was identified as its direct target through luciferase report assay. Age-related miR-708-5p deficiency increased sensitivity of CPCs for exposure to FFSS by liberating TLR4 expression. Intra-articular delivery agomiR-708-5p alleviated TMJ osteoarthritic cartilage lesions in mice. In conclusion, age-related miR-708-5p deficiency increases the sensitivity to mechanical loading stress and promotes CPCs senescence like degeneration via TLR4.

2023-07-11 | GSE236978 | GEO

2023-07-11 | GSE236977 | GEO

miR-181a modulates Acute Myeloid Leukemia susceptibility to natural killer cells

Project description:Overexpression of miR-181a in AML blasts: DNA Microarray was performed to compare overall gene expression profiles of KG-1 Anti-miR-CT and U937 Anti-miR-CT cells compared respectively to KG-1 Anti-miR-181a and U937 Anti-miR-181a.

2014-12-30 | E-MTAB-2837 | biostudies-arrayexpress

Identification of miR-181a target genes in Epithelial Ovarian Cancer

Project description:We have identified a single miRNA, miR-181a, that can modulate TGF-Î² signaling to induce and maintain EMT, and effect further downstream events of tumour cell survival, altered response to chemotherapy, migration, invasion and dissemination in vivo. Our present study provides an understanding of how enhanced expression of miR-181a can confer malignant and invasive traits through the modulation of a canonical signaling pathway and a consequent maintenance of a mesenchymal state. Furthermore, inhibition of miR-181a led to a reversion of EMT and subsequent events through decreased TGF-Î² signaling. Our data confirmed Smad7 as a functional target through which TGF-Î²-mediated EMT occurs; re-expression of Smad7 lacking its 3'UTR was able to rescue miR-181a-mediated phenotypes, deeming Smad7 as a critical mediator of miR-181a-induced EMT. Other recent studies support the crucial role(s) that miRNAs play in mediating EMT and consequent aggressive disease traits. For example, the miR-106b-25 cluster has also been shown to target Smad7 and mediate TGF-Î²-induced EMT downstream to Six1 in breast cancer34. miR-9 directly targets E-cadherin and inhibition of miR-9 had led to an inhibition of metastasis35. Conversely, the miR-200 and -205 family was shown to target transcriptional repressors of E-cadherin, ZEB1 and SIP1, and re-expression of these miRNAs led to a mesenchymal-to-epithelial transition and prevented TGF-Î² -induced EMT36. A2780 ovarian cancer cell lines stably expressing either pBABE (control vector), p181a#1( clone 1 expressing miR-181a) or p181a#2( clone 2 expressing miR-181a)

2013-12-01 | E-GEOD-52077 | biostudies-arrayexpress

Comparison of miR-181a transfected K562 cells and mock transfected K562 cells

Project description:This series consists of samples taken from two groups of K562 cells(miR-181a transfected group and control group ) and harvested 48 hours later. We used Agilent human 1A oligo microarray identified the changes in gene expression profile of K562 cells after miR-181a transfection experiment. Further studies aimed to find target mRNA of miR-181a in mammalian cells and its biological function. Keywords = miR-181a Keywords = microarray Keywords = K562 Keywords: microRNA transfection analysis

2005-11-18 | GSE3605 | GEO

miR-138 controls interneuron function and short-term memory

Project description:Using a miR-138 loss-of-function mouse model, a role for the brain enriched microRNA miR-138 in the regulation of inhibitory synaptic transmission and short-term memory formation was shown.

2022-04-06 | GSE173982 | GEO

Identification of miR-181a target genes in Epithelial Ovarian Cancer

Project description:We have identified a single miRNA, miR-181a, that can modulate TGF-β signaling to induce and maintain EMT, and effect further downstream events of tumour cell survival, altered response to chemotherapy, migration, invasion and dissemination in vivo. Our present study provides an understanding of how enhanced expression of miR-181a can confer malignant and invasive traits through the modulation of a canonical signaling pathway and a consequent maintenance of a mesenchymal state. Furthermore, inhibition of miR-181a led to a reversion of EMT and subsequent events through decreased TGF-β signaling. Our data confirmed Smad7 as a functional target through which TGF-β-mediated EMT occurs; re-expression of Smad7 lacking its 3'UTR was able to rescue miR-181a-mediated phenotypes, deeming Smad7 as a critical mediator of miR-181a-induced EMT. Other recent studies support the crucial role(s) that miRNAs play in mediating EMT and consequent aggressive disease traits. For example, the miR-106b-25 cluster has also been shown to target Smad7 and mediate TGF-β-induced EMT downstream to Six1 in breast cancer34. miR-9 directly targets E-cadherin and inhibition of miR-9 had led to an inhibition of metastasis35. Conversely, the miR-200 and -205 family was shown to target transcriptional repressors of E-cadherin, ZEB1 and SIP1, and re-expression of these miRNAs led to a mesenchymal-to-epithelial transition and prevented TGF-β -induced EMT36.

2013-12-01 | GSE52077 | GEO

Identification of the downstream target genes of miR-138 in gastric cancer

Project description:Our data showed that EIF4EBP1, NINJ1, CLIC3, STMN3, SPINK4, CD44, GSN, PRSS23 et al. were strongly downregulated by miR-138-mimics in gastric cancer (GC) cell lines. Besides, miR-138-5p has a profound effect on EMT signaling and proliferation signaling. In the EMT signaling, miR-138-5p negatively regulates the expression of SOX4, VIM, TGFB1, BMP1, ECM1 and CXCL8; In the cell proliferation signaling, miR-138-5p could negatively regulates the expression of PCNA, RHOC and CCND3.

2021-10-08 | GSE183654 | 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