Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A BAFF/APRIL axis regulates obesogenic-diet driven weight gain

ABSTRACT: Purpose: To define the role of the BAFF/APRIL axis in the regulation of adipose tissue homeostasis through RNAseq. Methods: Primary adipocytes were derived from pre-adipocyte precursors of inguinal white adipose from male C57BL/6 mice aged 6-8 weeks. Adipocytes were treated with rBAFF, rAPRIL, or multiple controls for 24 hours. mRNA profiles were generated for each condition, run in biological duplicates, using Illumina HiSeq2000 with single-end, 50bp reads. Differential gene lists were generated by comparing BAFF and APRIL to controls using unpaired ttests. Results:Following mapping an average of 30million reads across 10 samples to the mm10 mouse genome with annotations from UCSC, differential analysis identified genes involved in adipocyte pathways associated with lipid metabolism, lipolysis, and inflammation. Conclusion: BAFF and APRIL modulate modulate white adipocyte lipid handling.

ORGANISM(S): Mus musculus

PROVIDER: GSE131298 | GEO | 2021/02/08

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

BAFF and APRIL counterregulate susceptibility to inflammation-induced preterm birth

Project description:Emerging clinical evidence points to a function for B cell activating factor (BAFF) in pregnancy. However, a direct role for BAFF-axis members including BAFF, the closely related a proliferation-inducing ligand (APRIL), and their respective receptors in pregnancy has not been examined. This study demonstrates that loss of BAFF results in decreased inflammatory responsiveness and decreased susceptibility to inflammation-induced preterm birth (PTB). In contrast, loss of APRIL increases inflammatory responsiveness and susceptibility to PTB. Consistent with overlapping receptor utilization by BAFF and APRIL, deletion of BAFF-axis receptors is not sufficient to modify susceptibility to PTB. Critically, therapeutic administration of BAFF/APRIL monoclonal antibodies or recombinant proteins is sufficient to manipulate susceptibility to inflammation-induced PTB. Further, macrophages are identified as the principle BAFF producing immune cells at the maternal-fetal interface and BAFF and APRIL divergently manipulate macrophage gene expression and inflammatory function. Genes linked to labor initiation are upregulated in WT and APRIL deficient macrophages while downregulated in BAFF deficient macrophages and correlate with myeloid gene expression in human placental samples during labor. Thus, BAFF and APRIL play important, but divergent, counterregulatory inflammatory roles in pregnancy and provide new therapeutic targets for mitigating the risk of PTB.

2023-08-03 | GSE202811 | GEO

A BAFF/APRIL axis regulates obesogenic-diet driven weight gain

Project description:A BAFF/APRIL axis regulates obesogenic-diet driven weight gain

| PRJNA543147 | ENA

BAFF neutralization impairs the clearance of dead adipocytes and promotes insulin resistance in obese mice

Project description:B cell-activating factor (BAFF) is critical for the survival and maturation of B2 cells. However, excess BAFF breaks the peripheral tolerance of B2-cells leading to the production of autoantibodies that cause autoimmune diseases. During obesity, BAFF is predominantly produced by white adipose tissue (WAT), and IgG autoantibodies against adipocytes are identified in the WAT of obese humans. However, it remains to be determined if the autoantibodies formed during obesity affect WAT remodeling and systemic insulin resistance. Here, we show that IgGs from high-fat diet (HFD)-induced obese mice bind to apoptotic adipocytes and promote their clearance by macrophages. Next, using murine models of obesity in which the gonadal WAT undergoes remodeling, unexpectedly we found that BAFF neutralization increased the number of dead adipocytes and exacerbated WAT inflammation and insulin resistance despite depletion of IgG autoantibodies. RNA sequencing of the stromal vascular fraction from the WAT revealed impaired B cell activation and phagocytosis pathways. In-vitro, the clearance of apoptotic adipocytes by macrophages was attenuated in the presence of IgGs from BAFF-neutralized mice compared to the control mice. Altogether, our study suggests a beneficial role of BAFF and IgG autoantibodies in WAT remodeling in obesity and the regulation of systemic insulin resistance.

2024-08-28 | GSE255950 | GEO

BAFF and APRIL counterregulate susceptibility to inflammation-induced preterm birth

Project description:BAFF and APRIL counterregulate susceptibility to inflammation-induced preterm birth

| PRJNA837296 | ENA

A BAFF/APRIL axis regulates obesogenic diet-driven weight gain.

Project description:The impact of immune mediators on weight homeostasis remains underdefined. Interrogation of resistance to diet-induced obesity in mice lacking a negative regulator of Toll-like receptor signaling serendipitously uncovered a role for B cell activating factor (BAFF). Here we show that overexpression of BAFF in multiple mouse models associates with protection from weight gain, approximating a log-linear dose response relation to BAFF concentrations. Gene expression analysis of BAFF-stimulated subcutaneous white adipocytes unveils upregulation of lipid metabolism pathways, with BAFF inducing white adipose tissue (WAT) lipolysis. Brown adipose tissue (BAT) from BAFF-overexpressing mice exhibits increased Ucp1 expression and BAFF promotes brown adipocyte respiration and in vivo energy expenditure. A proliferation-inducing ligand (APRIL), a BAFF homolog, similarly modulates WAT and BAT lipid handling. Genetic deletion of both BAFF and APRIL augments diet-induced obesity. Lastly, BAFF/APRIL effects are conserved in human adipocytes and higher BAFF/APRIL levels correlate with greater BMI decrease after bariatric surgery. Together, the BAFF/APRIL axis is a multifaceted immune regulator of weight gain and adipose tissue function.

| S-EPMC8131685 | biostudies-literature

Transcriptomics to discover splice variants involved in the browning of adipose tissue

Project description:Adipose tissue is the major depot for energy storage. Recent studies have shown that at least three types of adipocytes can be distinguished depending on their anatomical locations : 1) The classic brown adipocytes, i.e., brown adipose tissue (BAT); 2) The 'brite' (brown-in-white) adipocytes, i.e. inguinal white adipose tissue (iWAT); 3) The 'true' white adipocytes, i.e., epididymal white adipose tissue (eWAT). Two strains of mice (SV129 and C57BL/6J) were used in this study. SV strain is resistant to obesity and latter is prone to obesity. Pre-adipocyte cells were isolated from subcutaneous tissue (iWAT) to create four groups of cell cultures per strain of mouse.

2016-04-20 | GSE57903 | GEO

A non-cell autonomous mechanism of beige adipocyte renaissance in subcutaneous adipose tissue

Project description:Two types of UCP1 positive cells-brown and beige adipocytes exist in mammals. Beige adipocytes are very plastic, and can be dynamically regulated by environment.Beige adipocytes formed postnatally in subcutaneous inguinal white adipose tissue (iWAT) lost thermogenic gene expression and multilocular morphology at adult stage, but cold could restore their “beigeing” characteristics, a phenomenon termed as beige adipocyte renaissance. Our results showed that beige cell maintenance and renaissance in adult mice were regulated by cAMP and HDAC4 signaling in white adipocytes non-cell autonomously. Genetic modulations of various components of this cAMP-HDAC4 cascade (e.g. LKB1) led to persistent browning and reduced adiposity independent of thermogenesis. To further study the mechanisms of beige adipocytes maintenance, we performed RNA-seq with samples from inguinal white adipose tissues of WT, AdipoqCre LKB1 F/F, and AdipoqCre LKB1 F/F; HDAC4 F/F mice.Our studies will move the beige adipocyte field forward and attract clinical applications to target beige adipocyte renaissance.

2018-02-14 | GSE85335 | GEO

Gene expression of adipocyte and stromal-vascular fractions

Project description:In order to select mRNA transcripts strongly enriched in murine white adipocytes versus brown adipocytes or stromal-vascular fraction, gene expression data of the adipocyte and stromal-vascular fractions of the interscapular brown, inguinal subcutaneous as well as visceral epididymal adipose tissue depots of young adult male C57BL/6 mice housed at constant 23Â°C ambient temperature were obtained. 18 samples: 3 different adipose tissues separated into stromal-vascular fraction and adipocytes, analyzed in biological triplicates.

2013-04-27 | E-GEOD-44059 | biostudies-arrayexpress

Transcriptomics profile of adipose and adipocyte with Gls perturbation

Project description:We generated single nucleus transcriptomic atlas for white and brown adipose tissue from adipocyte-specific Gls knockout mouse, and also generated bulk RNA-seq from in vitro differentiated human white adipocytes with/without GLS knock down.

2024-05-18 | GSE267800 | GEO

mRNA profiling of white hMADS cells converted in brite adipocytes and transfected with mimic miR-125b-5p

Project description:miR-125b-5p is a well known miRNA already describded in several forms of cancer. miR-125b-5p is expressed in adipose tissue, adipocytes as well as their precursor cells. We aim to invest the role of miR-125b-5p in white adipocytes conversion into brite adipocytes. To get an idea about putative targets of miR-125b-5p in adipocyte conversion, we transfected miR-125b-5p mimic in human Multipotent Adipose-Derived Stem (hMADS) cells, differenciated in white adipocytes. Gene expression profiling is performed 48h after hMADSC transfection.

2016-07-01 | GSE80816 | 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