Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Impact of a pro-inflammatory stimulus on the miRNA composition of extracellular vesicles (EV) from stem cells from apical papilla (SCAP)

ABSTRACT: To investigate the impact of a pro-inflammatory stimulus (TNFα and IFNγ, 20 ng/ml) on miRNA in SCAP-EV, we isolated EV from non-activated and activated SCAP and then extracted miRNA

ORGANISM(S): Homo sapiens

PROVIDER: GSE208577 | GEO | 2022/07/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Impact of a pro-inflammatory stimulus on the miRNA composition of extracellular vesicles (EV) from stem cells from apical papilla (SCAP)

Project description:Impact of a pro-inflammatory stimulus on the miRNA composition of extracellular vesicles (EV) from stem cells from apical papilla (SCAP)

| PRJNA860164 | ENA

Transcriptional Profliing of small molecules induced endothelial cells of stem cells from apical papilla (SCAP-ECs), stem cells from apical papilla (SCAP) and human vein endothelial cells (HUVECs)

Project description:Recently, a new strategy has been developed to directly reprogram one cell type towards targeted cell type by using different combinations of small molecule compounds. Here we attempted to induce stem cells from apical papilla (SCAP) into endothelial cells (ECs) by the same strategy. We developed a set of small molecules and growth factors that facilitates the conversion of SCAP into stable endothelial lineage. The SCAP-derived endothelial cells (SCAP-ECs) expressed some up-regulated endothelial specific genes and proteins, exhibited the ability to form functional tubular-like structures in vitro, and contributed to generate blood vessels in vivo. The aim of this study is to compare the ECs-related gene profile of SCAP, SCAP-derived ECs and HUVECs (primary ECs) and to explore whether SCAP-derived ECs showed enriched ECs gene expression.

2021-12-31 | GSE149930 | GEO

Expression data of microRNA from human stem cells from apical papilla

Project description:Osteo/odontogenic differentiation is a key process of human stem cells from apical papilla (SCAP) in tooth root development. Emerging evidence indicates microRNAs (miRNAs) play diverse roles in osteogenesis. However, their functions in osteo/odontogenic differentiation of SCAP remain to be elucidated. We used miRNA microarray to analysis differentially expressed miRNAs in order to investigate the role of miRNAs in SCAP osteo/odontogenic differentiation and underlying mechanism.

2021-01-01 | GSE154466 | GEO

Transcriptional Profliing of small molecules induced endothelial cells of stem cells from apical papilla (SCAP-ECs), stem cells from apical papilla (SCAP) and human vein endothelial cells (HUVECs)

Project description:Transcriptional Profliing of small molecules induced endothelial cells of stem cells from apical papilla (SCAP-ECs), stem cells from apical papilla (SCAP) and human vein endothelial cells (HUVECs)

| PRJNA630583 | ENA

MPC EV miRNA Microarray

Project description:MPC EV miRNA Microarray

| PRJNA641860 | ENA

Extracellular vesicle (EV) miRNome profiling in hiPSC-cardiomyocyte differentiation reveals a stemness-maintenance miRNA cluster driving hiPSC-EV bioactivity

Project description:Extracellular Vesicles (EV) are an attractive therapy to boost cardiac regeneration. Nevertheless, identification of EV and corresponding cell platform(s) suitable for therapeutic application, is still a challenge. Here, we isolated EV from key stages of the human induced pluripotent stem cell-cardiomyocyte (hiPSC-CM) differentiation and maturation, i.e., from hiPSC (hiPSC-EV), cardiac progenitors (CPC-EV), immature (CMi-EV) and mature (CMm-EV) cardiomyocytes, with the aim of identifying a promising cell biofactory for EV production, and pinpoint the genetic signatures of bioactive EV. EV were characterized in terms of expression of specific markers, yield, and size. Bioactivity was assessed in human umbilical vein endothelial cells (HUVEC) and hiPSC-CM. Small RNA-Seq was performed to identify the differentially expressed miRNA in the four EV groups. Bioactivity assays showed increased tube formation and migration in HUVEC treated with hiPSC-EV compared to EV from committed cell populations. hiPSC-EV also significantly increased hiPSC-CM proliferation. Global miRNA expression profiles corroborated an EV-miRNA pattern indicative of stem cell to cardiomyocyte specification. A stemness maintenance miRNA cluster upregulated in hiPSC-EV was found to target the PTEN/PI3K/AKT pathway. Moreover, hiPSC-EV treatment mediated PTEN suppression and increased AKT phosphorylation. Overall, our findings validate hiPSC as suitable cell biofactories for EV production for cardiac regenerative applications.

2022-06-01 | GSE179323 | GEO

Deletion of Scap in Alveolar Type II Cells Influences Lung Lipid Homeostasis and Identifies a Compensatory Role for Pulmonary Lipofibroblasts

Project description:Pulmonary function after birth is dependent upon surfactant lipids that reduce surface tension in the alveoli. The sterol-responsive element-binding proteins (SREBPs) are transcription factors regulating expression of genes controlling lipid homeostasis in many tissues. To identify the role of SREBPs in the lung, we conditionally deleted the SREBP cleavage-activating protein gene, Scap, in respiratory epithelial cells (Scap∆/∆) in vivo. Prior to birth (E18.5), deletion of Scap decreased the expression of both SREBPs and a number of genes regulating fatty acid and cholesterol metabolism. Nevertheless, Scap∆/∆ mice survived postnatally, surfactant and lung tissue lipids being substantially normalized in adult Scap∆/∆ mice. Although phospholipid synthesis was decreased in type II cells from adult Scap∆/∆ mice, lipid storage, synthesis, and transfer by lung lipofibroblasts were increased. mRNA microarray data indicated that SCAP influenced two major gene networks, one regulating lipid metabolism and the other stress-related responses. Deletion of the SCAP/SREBP pathway in respiratory epithelial cells altered lung lipid homeostasis and induced compensatory lipid accumulation and synthesis in lung lipofibroblasts. To identify the role of SREBPs in the lung, we conditionally deleted the SREBP cleavage-activating protein gene, Scap, in respiratory epithelial cells (Scap∆/∆) in vivo.Lung cRNA was hybridized to the murine genome MOE430 V2 chips.

2011-01-08 | E-GEOD-26496 | biostudies-arrayexpress

Liver gene expression profile of wild type, liver-specific PTEN KO, SCAP KO and PTEN/SCAP double KO mice.

Project description:Nonalcoholic steatohepatitis (NASH), a severe form of nonalcoholic fatty liver disease, is characterized by hepatic steatosis and hepatocellular injury and progresses to cirrhosis and hepatocellular carcinoma. Sterol regulatory element-binding proteins (SREBPs) are master regulators of lipogenesis. Liver-specific PTEN knockout (KO) mice show constitutive upregulation of SREBP through PI3K-Akt pathway activation, leading to spontaneous fatty liver and subsequent HCC development. SREBP cleavage-activating protein (SCAP) plays a critical role in SREBP activation. We sought to determine the impact of SREBP inhibition on NASH and HCC development. To this end, we additionally inhibited SREBP pathway in liver-specific PTEN mice by ablating SCAP and generated liver-specific PTEN/SCAP double KO (DKO) mice. However unexpectedly, inhibition of SCAP/SREBP pathway markedly exacerbated liver injury (5weeks), fibrosis (5months), and carcinogenesis (7 months) in PTEN KO mice. To elucidate the mechanisms of liver injury in liver-specific PTEN/SCAP DKO mice, we conducted transcriptome analyses of the livers.

2022-04-05 | GSE169104 | GEO

The expression profiling comparison of mice with Scap and Insig deletion from perinatal lung (E17.5-PN1)

Project description:In this study, we studied the genomic responses of the Insig and Scap deletion from perinatal lung. Through comprehensive data analysis and integration, time dependent effects of epithelial SCAP/INSIG/SREBP deletion and defined SCAP/INSIG/SREBP-associated genes, bioprocesses and downstream pathways were identified. Total lung RNA was isolated from Scapdelata/delta, Insig1/2delta/delta, and respective control littermates at E17.5, E18.5 and PN1 were used for mRNA expression profiling analysis (n=3 for each condition)

2014-07-10 | E-GEOD-53397 | biostudies-arrayexpress

Variability of bovine milk EV measurements in health and subclinical mastitis

Project description:Mastitis, the inflammation of the mammary gland, is one of the most prevalent diseases in dairy farming worldwide. Unfortunately, the disease is most often present in a subclinical type with no clear symptoms. The sooner the infection is detected, the less opportunities for the disease to progress and the more treatment options remain available. Milk microRNA (miRNA) encapsulated in extracellular vesicles (EV) have been proposed as potential biomarkers of different mammary gland conditions, including subclinical mastitis. However, little is known about the robustness of EV analysis regarding sampling time-point or natural infections. In order to estimate the reliability of EV measurements in raw bovine milk, we first evaluated the changes in EV size, concentration and miRNA cargo during three consecutive days. Then, we compared milk EV differences from natural infected quarters with high somatic cell count (SCC) with their healthy adjacent quarters with low SCC and quarters from uninfected udders. We found that milk EV miRNA cargo is very stable along three days and that infected quarters do not induce relevant changes in milk EV of adjacent healthy quarters, making them suitable controls. We observed cow-individual changes in immunoregulatory miRNA in quarters with chronic subclinical mastitis, pointing towards infection-specific alterations. Finally, we proposed bta-miR-223 as a potential indicator of subclinical mastitis prognosis in raw milk.

2022-03-16 | GSE149856 | 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