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Liver gene expression profile in mice (C57Bl/6J) lacking ATGL in white adipose tissue in response to feeding, fasting or beta 3 adrenergic stimulation with CL316243

ABSTRACT: Adipocyte-specific Atgl knockout (Atgladipo-/-) mice were bred at the animal facility of the University of Graz. They were originally generated at the animal facility of the University of Pittsburgh by mating the floxed-Atgl mouse strain with Adiponectin-Cre mice to obtain Cre+/−Atglflox/flox mice (AAKO). Cre-/-Atglflox/flox mice (Atgladipo+/+) were used as controls (CTRL).

ORGANISM(S): Mus musculus

PROVIDER: GSE165699 | GEO | 2022/09/15

REPOSITORIES: GEO

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RNA-seq analysis of lung-infiltrating neutrophils from WT and Atgl-cKO mice

Project description:Atglflox/flox (B6N.129S-Pnpla2tm1Eek/J), S100A8-cre+/- (B6.Cg-Tg(S100A8-cre,-EGFP)1Ilw/J) mice were obtained from The Jackson Laboratory. Atglflox/flox mice were bred to S100A8-cre+/- mice to generate Atglflox/WTS100A8-cre+/- mice, which were backcrossed onto Atglflox/flox mice to generate Atglflox/floxS100A8-cre+/- mice (Atgl neutrophils-specific knock out, Atgl-cKO). Age-matched littermate Atglflox/flox mice were used as wild-type (WT) controls. To compare of the gene expression of the lung-infiltrating neutrophils isolated from Atgl-cKO mice and their WT littermates, AT3-g-csf cells were injected into the fourth mammary fat pads of female WT and Atgl-cKO mice (10-week-old, n = 4/group). The AT3-g-csf cell line is based on a murine breast cancer cell line (AT3) derived from MMTV-PyMT tumors in the C57BL/6 background, and further constructed to overexpress granulocyte-colony stimulating factor (G-CSF) for induction of the host inflammatory condition. At day 10 (pre-metastatic stage), the mice were euthanized and then Ly6G+ neutrophils were isolated from lung by using anti-Ly6G MicroBead Kit (Miltenyi Biotec) following manufacturer’s instructions. The isolated neutrophils were analyzed by flow cytometry and the cells with a > 95% purity were used for the next procedure. Total RNA was isolated from neutrophils using the miRNeasy Mini kit (Qiagen) and the transcriptional profiles of neutrophils were analyzed by RNA sequencing.

2020-06-28 | E-MTAB-9235 | biostudies-arrayexpress

Effect of beta3 adrenergic activation on liver gene expression profile in mice (C57Bl/6J) expressing hepatocyte PPARalpha or not

Project description:Pparα hepatocyte-specific knockout (Pparαhep-/-) mice were generated at INRAE’s rodent facility (Toulouse, France) by mating the floxed-Pparα mouse strain with C57BL/6J albumin-Cre transgenic mice to obtain albumin-Cre+/-Pparαflox/flox mice (LKO). Albumin-Cre-/-Pparαflox/flox (Pparαhep+/+) littermates were used as controls (LWT). Twelve week-old mice were transferred in a ventilated cabinet at the specific temperature of 30°C (thermoneutrality) 2 weeks before experiments. Mice were fed ad libitum or fasted at ZT0 and given beta3 adrenergic receptor agonist: CL316243 ((3 mg/kg body weight; Sigma Aldrich) = Beta3) or vehicle (0.5% carboxymethyl cellulose in sterilized water)=vehicle) by gavage at ZT10 and sacrificed at ZT16.

2022-09-15 | GSE165558 | GEO

The proteomic study on kidney-specific Tmod1 knockout mice

Project description:We performed proteomic analyses on the kidneys of Tmod1 flox/flox/Ksp-Cre- (TF) and Tmod1 flox/flox/Ksp-Cre+ (TFK) mice.

2019-06-10 | MSV000083953 | MassIVE

Transcription profiling of six tissues from ATGL knock-out versus wild type mice

Project description:Gene expression profiling in 6 tissues (white adipose tissue (WAT), brown adipose tissue (BAT), cardiac muscle (CM), liver (LIV), kidney (KID), skeletal muscle (SM)) from ATGL(-/-) mice versus wildtype (ATGL+/+) mice.

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Expression data from Club cells of wt/cTg and Atgl KO/cTg

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ATGL deletion in castration-resistant prostate cancer cell line

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2023-11-22 | GSE243159 | GEO

Effect of ATGL knockdown by siRNA in human umbilical vein endothelial cells

Project description:To investigate the role of ATGL in endothelial cell function, we knockdown ATGL with siRNA and compared with siCTL. We then performed gene expression profiling analysis using data obtained from RNA-seq of 3 different samples each condition.

2023-11-03 | GSE231619 | GEO

Elevated ATGL in colon cancer cells and cancer stem cells promotes metabolic and tumorigenic reprogramming reinforced by obesity

Project description:Obesity is a worldwide epidemic associated with increased risk and progression of colon cancer. Here, we aimed to determine the role of adipose triglyceride lipase (ATGL), responsible for intracellular lipid droplet (LDs) utilization, in obesity driven colonic tumorigenesis. In local colon cancer patients, significantly increased ATGL levels in tumor tissue, compared to controls, were augmented in obese individuals. Elevated ATGL levels in human colon cancer cells (CCC) relative to non-transformed were augmented by an obesity mediator, oleic acid (OA). In CCC and colonospheres, enriched in colon cancer stem cells (CCSC), inhibition of ATGL prevented LDs utilization and inhibited OA-stimulated growth through retinoblastoma-mediated cell-cycle arrest. Further, transcriptomic analysis of CCC, with inhibited ATGL, revealed targeted pathways driving tumorigenesis and high-fat-diet obesity facilitated tumorigenic pathways. Inhibition of ATGL in colonospheres revealed targeted pathways in human colonic tumor crypt base cells (enriched in CCSC) derived from colon cancer patients. In CCC and colonospheres, we validated selected transcripts targeted by ATGL inhibition, some with emerging roles in colonic tumorigeneses (ATG2B, PCK2, PGAM1, SPTLC2, IGFBP1, ABCC3) and others with established roles (MYC, MUC2). These findings demonstrate obesity-promoted, ATGL-mediated colonic tumorigenesis and establishes therapeutic significance of ATGL in obesity reinforced colon cancer progression.

2022-02-05 | GSE195994 | GEO

Quantitative proteomic analysis of the livers from 5-week-old HyD-LIRflox/flox and HyD-LIRflox/flox; Alb-Cre mice.

Project description:We have previously shown that the HyD-LIR-Venus probe can specifically inhibit selective autophagy by suppressing the interaction of LIR-containing selective autophagy substrates and receptors with ATG8-family proteins in vivo. We generated hepatocyte-specific HyD-LIR-Venus-expressing mice (HyD-LIRflox/flox; Alb-Cre) by crossing HyD-LIRflox/flox mice, in which HyD-LIR-Venus is expressed under CAG promoter in a Cre-recombinase-dependent manner, with Alb-Cre transgenic mice that express Cre under the control of the Albumin promoter. We performed quantitative proteomic analysis of the livers of 5-week-old HyD-LIRflox/flox and HyD-LIRflox/flox; Alb-Cre mice using the RTS-SPS-MS3 method on Tribrid mass spectrometry.

2023-04-24 | PXD037013 | JPOST Repository

Genome-wide analysis of gene expression in normal and fibrotic mouse kidneys with and without Twist1 or with and without Snai1(Snail) expression in proximal tubular epithelial cells

Project description:In this study mice were engineered to specifically delete Twist1 or Snail expression in proximal tubular epithelial cells of the kidney (ggt-cre+;Twist flox/flox and ggt-cre+;Snail flox/flox ). These mice and control mice (ggtcre-;Twist flox/flox: these express Twist1, and ggtcre-;Snail flox/flox:these express Snail) were subjected to unilaterial ureteric obstruction. This experiment allows for the collection and analysis of expression in contralateral healthy (HK) kidney adn obstructed disease (DK) kidney. Total RNA was isolated from the contralateral healthy (HK) and obstructed disease (DK) kidneys of 3 mice with ggt-cre-;Twist flox/flox genotype (Wildtype like) and 4 mice with ggt-cre+;Twist flox/flox genotype (loss of Twist1 in proximal tubular epithelial cells), 3 mice with ggt-cre-;Snail flox/flox genotype (Wildtype like) and 3 mice with ggt-cre+;Snail flox/flox genotype (loss of Snail in proximal tubular epithelial cells). Total RNA was also isolated from kidneys of completely healthy mice: 3 mice ggt-cre-;WT, 3 mice ggt-cre+;WT, 3 mice ggt-cre+;Twist flox/flox and 3 ggt-cre+;Snail flox/flox

2015-08-03 | E-GEOD-60685 | biostudies-arrayexpress

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