Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MicroRNA expression profile of the SVF of visWAT under β3-adrenegic stimulation

ABSTRACT: microRNA expression profile of the SVF of visWAT under β3-adrenegic stimulation

PROVIDER: PRJNA415065 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

microRNA expression profile of the SVF of visWAT under β3-adrenegic stimulation

Project description:We used microRNA expression analysis to identify which microRNAs are expressed in the stromal vascular fraction (SVF) of visceral white adipose tissue (visWAT) to identify of microRNA expression patterns are changed upon CL-316,243 treatment Agilent mouse miRNA microarray (Cat. No. G4872A-046065, Agilent Technologies) was performed on the SVF of visWAT of 8-week-old C57/BL6 mice treated with CL 316243 or Vehicle (PBS) for three days. Isolated miRNA and total RNA was used for array analysis by Shanghai Biotechnology Corporation. Normalization and analysis for differentially expressed genes were performed using robust multi-array analysis and significance analysis of microarrays (SAM) via R statistical software packages “oligo” and “samr”. Several up- and downregulated microRNAs could be identified and were further varified with qPCR and compared with mRNA expression levels of their main targets.

2017-10-20 | GSE105226 | GEO

Ileal Crohn’s disease exhibits reduced activity of phospholipase C-β3 (PLC-β3)-dependent Wnt/b-catenin signaling pathway [microarray]

Project description:Crohn’s disease is a chronic, debilitating inflammatory bowel disease. Here we report a critical role for phospholipase C-β3 (PLC-β3) in intestinal homeostasis. In PLC-β3- deficient mice, exposure to oral dextran sodium sulfate induced lethality and severe inflammation in the small intestine. The lethality was due to PLC-β3 deficiency in multiple non-hematopoietic cell types. PLC-β3 deficiency resulted in reduced Wnt/β-catenin signaling, which is essential for homeostasis and regeneration of the intestinal epithelium. PLC-β3 regulated the Wnt/β-catenin pathway in small intestinal epithelial cells (IECs) at transcriptional, epigenetic, and potentially protein-protein interaction levels. PLC-β3- deficient IECs were unable to respond to stimulation by R-spondin 1, an enhancer of Wnt/β-catenin signaling. Reduced expression of PLC-β3 and its signature genes was found in biopsies of ileal Crohn’s disease patients. PLC-β regulation of Wnt signaling was evolutionally conserved in Drosophila. Our data indicate that reduction of PLC-β3- mediated Wnt/β-catenin signaling contributes to the pathogenesis of ileal Crohn’s disease.

2024-10-06 | GSE244937 | GEO

Ileal Crohn’s disease exhibits reduced activity of phospholipase C-β3 (PLC-β3)-dependent Wnt/b-catenin signaling pathway [ATAC-Seq]

Project description:Crohn’s disease is a chronic, debilitating inflammatory bowel disease. Here we report a critical role for phospholipase C-β3 (PLC-β3) in intestinal homeostasis. In PLC-β3- deficient mice, exposure to oral dextran sodium sulfate induced lethality and severe inflammation in the small intestine. The lethality was due to PLC-3 deficiency in multiple non-hematopoietic cell types. PLC-β3 deficiency resulted in reduced Wnt/-catenin signaling, which is essential for homeostasis and regeneration of the intestinal epithelium. PLC-β3 regulated the Wnt/β-catenin pathway in small intestinal epithelial cells (IECs) at transcriptional, epigenetic, and potentially protein-protein interaction levels. PLC-β3- deficient IECs were unable to respond to stimulation by R-spondin 1, an enhancer of Wnt/β-catenin signaling. Reduced expression of PLC-β3 and its signature genes was found in biopsies of ileal Crohn’s disease patients. PLC-β regulation of Wnt signaling was evolutionally conserved in Drosophila. Our data indicate that reduction of PLC-β3- mediated Wnt/β-catenin signaling contributes to the pathogenesis of ileal Crohn’s disease.

2024-10-06 | GSE244935 | GEO

Ileal Crohn’s disease exhibits reduced activity of phospholipase C-β3 (PLC-β3)-dependent Wnt/b-catenin signaling pathway [16S rRNA]

Project description:Crohn’s disease is a chronic, debilitating inflammatory bowel disease. Here we report a critical role for phospholipase C-β3 (PLC-β3) in intestinal homeostasis. In PLC-β3- deficient mice, exposure to oral dextran sodium sulfate induced lethality and severe inflammation in the small intestine. The lethality was due to PLC-3 deficiency in multiple non-hematopoietic cell types. PLC-β3 deficiency resulted in reduced Wnt/-catenin signaling, which is essential for homeostasis and regeneration of the intestinal epithelium. PLC-β3 regulated the Wnt/β-catenin pathway in small intestinal epithelial cells (IECs) at transcriptional, epigenetic, and potentially protein-protein interaction levels. PLC-β3- deficient IECs were unable to respond to stimulation by R-spondin 1, an enhancer of Wnt/β-catenin signaling. Reduced expression of PLC-β3 and its signature genes was found in biopsies of ileal Crohn’s disease patients. PLC-β regulation of Wnt signaling was evolutionally conserved in Drosophila. Our data indicate that reduction of PLC-β3- mediated Wnt/β-catenin signaling contributes to the pathogenesis of ileal Crohn’s disease.

2024-10-06 | GSE244936 | GEO

Single cell sequencing of stromal vascular fraction (SVF) under B3-adrenergic agonist stimulation and mature adipocytes under cold exposure and B3-adrenergic agonist stimulation

Project description:A single cell suspension was generated from B3-adrenergic agonist (CL; 1 mg/kg/day) for 4 days and saline mouse SVF, and single-cell mRNAseq libraries were generated with Drop-Seq. A single cell suspension was generated from mouse mature adipocyte nuclei under the following conditions: RT, 24hrs @ 4 °C , 48hrs @ 4 °C, 4days @ 4 °C and B3-adrenergic agonist (CL; 1 mg/kg/day) and single-cell mRNAseq libraries were generated with 10X genomics.

2019-10-17 | GSE133486 | GEO

Single cell sequencing of stromal vascular fraction (SVF) under B3-adrenergic agonist stimulation and mature adipocytes under cold exposure and B3-adrenergic agonist stimulation

Project description:Single cell sequencing of stromal vascular fraction (SVF) under B3-adrenergic agonist stimulation and mature adipocytes under cold exposure and B3-adrenergic agonist stimulation

| PRJNA551597 | ENA

Human dendritic cell microRNA profile after NOD2 and / or TLR2 stimulation

Project description:microRNA expression in human monocyte-derived DCs following stimulation with NOD2 ligand MDP, TLR2 ligand Pam3CSK4, or both.

2013-06-01 | GSE44785 | GEO

Human Obese SVF

Project description:We compared the expression profile from human SVF of obese and lean patients (6 patient samples were pooled for one array)

2011-07-20 | E-MEXP-3313 | biostudies-arrayexpress

Human dendritic cell microRNA profile after NOD2 and / or TLR2 stimulation

Project description:microRNA expression in human monocyte-derived DCs following stimulation with NOD2 ligand MDP, TLR2 ligand Pam3CSK4, or both. 4 condition experiment with two timepoints, and 4 biological replicates. Conditions: unstimulated; MDP stimulated; Pam3CSK4 stimulated; MDP + Pam3CSK4 stimulated. Timepoints: 4 hours and 24 hours.

2013-06-01 | E-GEOD-44785 | biostudies-arrayexpress

Mechano-hypoxia conditioning with TGF-β3 withdrawal promotes stable, non-hypertrophic chondrogenesis of human mesenchymal stem cells

Project description:We hypothesize that the combination of mechanical loading with hypoxia culture and TGF-β3 growth factor withdrawal will promote stable, non-hypertrophic chondrogenesis of hBM-MSC embedded in an HA-hydrogel. To this end, we first assessed static hypoxia culture with growth factor withdrawal against static normoxia (20% O2) culture at the global transcriptome and tissue matrix level. We then assess two modalities of mechanical loading (dynamic compression, DC and cyclic hydrostatic pressure, CHP) with growth factor withdrawal against static culture, all under hypoxia. Results showed that Mechanical stimulation and TGF-β3 withdrawal under hypoxia promoted a strong chondrogenic and non-hypertrophic phenotype of hBM-MSC.

2023-04-19 | GSE214720 | 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