Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Dysregulation of Amyloid Precursor Protein impairs adipose tissue mitochondrial function and promotes obesity

ABSTRACT: Mitochondria from subcutaneous white adipose tissues of control or signal recognition particle 54c (SPR54c) transgenic mice were isolated and underwent further Percoll gradient-based purification. Purified mitochondria were subject to mass-spectrometry based proteomic analysis performed by UT Southwestern Proteomics Core. ID# 696496: SRP54c Transgenic; ID# 696497: control.

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Mus Musculus (ncbitaxon:10090)

SUBMITTER: Philipp Scherer

PROVIDER: MSV000084498 | MassIVE | Thu Oct 24 08:57:00 BST 2019

REPOSITORIES: MassIVE

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Dysregulation of Amyloid Precursor Protein Impairs Adipose Tissue Mitochondrial Function and Promotes Obesity.

Project description:Mitochondrial function in white adipose tissue (WAT) is an important yet understudied aspect in adipocyte biology. Here, we report a role for amyloid precursor protein (APP) in compromising WAT mitochondrial function through a high-fat diet (HFD)-induced, unconventional mis-localization to mitochondria that further promotes obesity. In humans and mice, obese conditions significantly induce APP production in WAT and its enrichment in mitochondria. Mechanistically, a HFD-induced dysregulation of signal recognition particle subunit 54c is responsible for the mis-targeting of APP to adipocyte mitochondria. Mis-localized APP blocks the protein import machinery, leading to mitochondrial dysfunction in WAT. Adipocyte-specific and mitochondria-targeted APP overexpressing mice display increased body mass and reduced insulin sensitivity, along with dysfunctional WAT due to a dramatic hypertrophic program in adipocytes. Elimination of adipocyte APP rescues HFD-impaired mitochondrial function with significant protection from weight gain and systemic metabolic deficiency. Our data highlights an important role of APP in modulating WAT mitochondrial function and obesity-associated metabolic dysfunction.

| S-EPMC6980705 | biostudies-literature

Adipose Precursor HO-1 prevents healthy visceral adipose tissue expansion during obesity[II]

Project description:Excessive accumulation of white adipose tissue (WAT) is a hallmark of obesity. The expansion of WAT in obesity involves proliferation and differentiation of adipose precursors (APs), however, the underlying molecular mechanisms remain unclear. Here, we identify Heme Oxygenase-1 (HO-1) as selectively being upregulated in the AP fraction of WAT, upon high-fat diet (HFD) feeding. Specific conditional deletion of HO-1 in APs of Hmox1fl/fl-Pdgfra Cre mice enhanced HFD-dependent visceral AP proliferation and differentiation, upstream of Cebpα and PPARγ. Opposite effects on human preadipocyte proliferation and differentiation in vitro were observed following HO-1 overexpression. Mechanistically, HO-1 acts upstream of AKT2 via ROS thresholding in mitochondria. Deletion of HO-1 in APs is sufficient to lower blood glucose, insulin and free fatty acid levels as well as liver steatosis during obesity, an effect not seen when HO-1 was conditionally deleted at later stages of adipogenesis using AdipoQ-Cre. Together, our data identify HO-1 as a diet-induced regulator limiting visceral adipose tissue hyperplasia during obesity.

2017-03-08 | GSE80147 | GEO

Adipose Precursor HO-1 prevents healthy visceral adipose tissue expansion during obesity [I]

2017-03-08 | GSE80146 | GEO

Subcutaneous adipose tissue and visceral adipose tissue gene expression profiles in Mexican patients with obesity

Project description:Using RNA isolated from subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) samples obtained from control and class I, II and III obese patients undergoing inguinal hernia repair and laparoscopic cholecystectomy, we compared the gene expression profiles between SAT and VAT using microarrays and validated the findings by real-time quantitative PCR.

2016-07-20 | GSE84599 | GEO

Subcutaneous adipose tissue and visceral adipose tissue gene expression profiles in Mexican patients with obesity

2016-07-20 | E-GEOD-84599 | biostudies-arrayexpress

Gene expression comparison in between mitoNEET transgenic vs wild type subcutaneous adipose tissue

Project description:mRNA expression was compared in between wild type and mitoNEET transgenic subcutaneous adipose tissue RNA was isolated from subcutaneous adipose tissue from male FVB mice in the light phase. mRNA expression was compared in between wild type and mitoNEET transgenic subcutaneous adipose tissue.

2012-07-11 | E-GEOD-39251 | biostudies-arrayexpress

A Memory for Obesity in Adipose Tissue

Project description:To identify transcriptional alterations in subcutaneous human white adipose tissue of post-obese subjects, global gene expression measurements were performed. Three groups, obese before and after bariatric surgery as well as never-obese controls, were compared to dissect candidate genes.

2017-06-01 | GSE59034 | GEO

Adipose tissue-specific dysregulation of angiotensinogen by oxidative stress in obesity.

Project description:Adipose tissue expresses all components of the renin-angiotensin system including angiotensinogen (AGT). Recent studies have highlighted a potential role of AGT in adipose tissue function and homeostasis. However, some controversies surround the regulatory mechanisms of AGT in obese adipose tissue. In this context, we here demonstrated that the AGT messenger RNA (mRNA) level in human subcutaneous adipose tissue was significantly reduced in obese subjects as compared with nonobese subjects. Adipose tissue AGT mRNA level in obese mice was also lower as compared with their lean littermates; however, the hepatic AGT mRNA level remained unchanged. When 3T3-L1 adipocytes were cultured for a long period, the adipocytes became hypertrophic with a marked increase in the production of reactive oxygen species. Expression and secretion of AGT continued to decrease during the course of adipocyte hypertrophy. Treatment of the 3T3-L1 and primary adipocytes with reactive oxygen species (hydrogen peroxide) or tumor necrosis factor alpha caused a significant decrease in the expression and secretion of AGT. On the other hand, treatment with the antioxidant N-acetyl cysteine suppressed the decrease in the expression and secretion of AGT in the hypertrophied 3T3-L1 adipocytes. Finally, treatment of obese db/db mice with N-acetyl cysteine augmented the expression of AGT in the adipose tissue, but not in the liver. The present study demonstrates for the first time that oxidative stress dysregulates AGT in obese adipose tissue, providing a novel insight into the adipose tissue-specific interaction between the regulation of AGT and oxidative stress in the pathophysiology of obesity.

| S-EPMC2891233 | biostudies-literature

Adipose tissue from β-3 agonist-treated mice

Project description:We previously established the transcription factor Zfp423 is critical for maintaining white adipocyte identity through suppression of the thermogenic gene program. The loss of Zfp423 in mature adipocytes triggers the rapid conversion of energy-storing white adipocytes into thermogenic beige adipocytes in subcutaneous WAT. In contrast to subcutaneous WAT, visceral WAT is relatively resistant to browning. However, visceral adipocytes lacing Zfp423 are capable of inducing the thermogenic gene program upon β-3 adrenergic stimulus. Here, we generated mice lacking Zfp423 in visceral adipose by breeding transgenic mice expressing Cre recombinase under the control of the Wilms Tumor 1 locus (Wt1-Cre) to animals carrying the floxed Zfp423 alleles (Zfp423loxP/loxP) (“Vis-KO” mice). Inactivation of Zfp423 in visceral WAT gives rise to thermogenic adipocytes that share properties of subcutaneous beige adipocytes and classic brown adipocytes.

2017-04-25 | GSE98132 | GEO

RNA-seq of mouse adipose stem and progenitor cells

Project description:Population control for the scRNA-seq based analysis a well-established fraction of mouse subcutaneous adipose-derived stromal vascular fraction (SVF) cells that is generally considered to harbour adipogenic stem and progenitor cells (ASPCs). We collected Lin- (CD31- CD45- TER119-) CD29+ CD34+ SCA1+ cells from the mouse subcutaneous SVF of transgenic mice, in which red fluorescent protein (RFP) is induced in Dlk1-expressing cells upon feeding with tamoxifen. While CD29, CD34, and SCA1 are generally expected to enrich for stem cells, DLK1 has previously been suggested to specifically mark pre-adipocytes.

2018-05-01 | E-MTAB-5818 | 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