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LSD1 complexes - Lsd1 Ablation Triggers Metabolic Reprogramming of Brown Adipose Tissue

ABSTRACT: Lsd1 ablation triggers metabolic reprogramming of brown adipose tissue. Lsd1 protein complexes were purified from mouse adipose tissue and analyzed by label-free LC-MS/MS. Mice were kept under different conditions prior complex isolation.

OTHER RELATED OMICS DATASETS IN: GSE81557PRJNA321981PRJNA321980PRJNA321978

INSTRUMENT(S): LTQ Orbitrap

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Brown Adipose Tissue

SUBMITTER: Joern Dengjel

LAB HEAD: Joern Dengjel

PROVIDER: PXD004745 | Pride | 2017-01-03

REPOSITORIES: Pride

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			Action	DRS
	20150204_KP_BAT_RT_4871_01.raw	Raw
	20150204_KP_BAT_RT_4871_02.raw	Raw
	20150204_KP_BAT_RT_4871_03.raw	Raw
	20150204_KP_BAT_RT_4871_04.raw	Raw
	20150204_KP_BAT_RT_4871_05.raw	Raw

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Publications

Lsd1 Ablation Triggers Metabolic Reprogramming of Brown Adipose Tissue.

Duteil Delphine D Tosic Milica M Lausecker Franziska F Nenseth Hatice Z HZ Müller Judith M JM Urban Sylvia S Willmann Dominica D Petroll Kerstin K Messaddeq Nadia N Arrigoni Laura L Manke Thomas T Kornfeld Jan-Wilhelm JW Brüning Jens C JC Zagoriy Vyacheslav V Meret Michael M Dengjel Jörn J Kanouni Toufike T Schüle Roland R

Cell reports 20161001 4

Previous work indicated that lysine-specific demethylase 1 (Lsd1) can positively regulate the oxidative and thermogenic capacities of white and beige adipocytes. Here we investigate the role of Lsd1 in brown adipose tissue (BAT) and find that BAT-selective Lsd1 ablation induces a shift from oxidative to glycolytic metabolism. This shift is associated with downregulation of BAT-specific and upregulation of white adipose tissue (WAT)-selective gene expression. This results in the accumulation of d ...[more]

PMID: 27760309

Similar Datasets

Lsd1 Ablation Triggers Metabolic Reprogramming of Brown Adipose Tissue.

Project description:Previous work indicated that lysine-specific demethylase 1 (Lsd1) can positively regulate the oxidative and thermogenic capacities of white and beige adipocytes. Here we investigate the role of Lsd1 in brown adipose tissue (BAT) and find that BAT-selective Lsd1 ablation induces a shift from oxidative to glycolytic metabolism. This shift is associated with downregulation of BAT-specific and upregulation of white adipose tissue (WAT)-selective gene expression. This results in the accumulation of di- and triacylglycerides and culminates in a profound whitening of BAT in aged Lsd1-deficient mice. Further studies show that Lsd1 maintains BAT properties via a dual role. It activates BAT-selective gene expression in concert with the transcription factor Nrf1 and represses WAT-selective genes through recruitment of the CoREST complex. In conclusion, our data uncover Lsd1 as a key regulator of gene expression and metabolic function in BAT.

| S-EPMC5081406 | biostudies-literature

Expression Profiles of miRNAs in brown fat of mice at room temperature and cold exposure (8C)

Project description:microRNAs levels were measured in brown adipose tissue of male C57Bl6N mice that were kept at RT or during cold exposure (8Â°C) for 24 hrs. Several miRNAs including myomirs were identified to be regulated in response to cold. Brown adipose tissue from 2 groups of 8 weeks old male C57Bl6N mice at room temperature (n=3) or after cold exposure n=3) at 8Â°C for 24 hrs were excised and RNA was extracted using Trizol and the manufactureres recommended procedure. miRNA expression levels were determined using Agilent microRNA expression analysis platform.

2012-11-01 | E-GEOD-41306 | biostudies-arrayexpress

LSD1 ablation stimulates anti-tumor immunity and enables checkpoint blockade

Project description:Chromatin regulators play a broad role in regulating gene expression, and when gone awry, can lead to cancer. Here we demonstrate that ablation of the histone demethylase LSD1 in cancer cells increases repetitive element expression, including ERVs, and decreases expression of RNA-induced silencing complex (RISC) components. Significantly, this leads to dsRNA stress and activation of type 1 interferon, which stimulates anti-tumor T cell immunity and restrains tumor growth. Furthermore, LSD1 depletion enhances tumor immunogenicity and T cell infiltration in poorly immunogenic tumors, and elicits significant responses of checkpoint blockade-refractory mouse melanoma to anti-PD-1 therapy. Consistently, TCGA data analysis shows an inverse correlation between LSD1 expression and CD8+ T cell infiltration in various human cancers. Our study identifies LSD1 as a potent inhibitor of anti-tumor immunity and responsiveness to immunotherapy, and suggests LSD1 inhibition combined with PD-(L)1 blockade as a novel cancer treatment strategy.

2018-06-21 | GSE112230 | GEO

Thermoneutrality acclaimed mouse interscapular brown and inguinal white adipose tissue

Project description:Adult mouse kept at 30C, RNAseq was performed for interscapular brown and inguinal white adipose tissue

2020-07-13 | E-MTAB-9062 | biostudies-arrayexpress

LSD1 knockdown in 3T3-L1 preadipocytes

Project description:Obesity is often associated with a low-grade systemic inflammation state that contributes to the development of insulin resistance and atherosclerotic complications. This is usually coupled with increased macrophage infiltration in the adipose tissue and a defect in adipocyte differentiation that results in accumulation of hypertrophic fat cells characterized by a deregulated pattern of adipokine expression. Here we show that knockdown of histone demethylase lsd1 in 3T3-L1 preadipocytes results in defective adipogenesis and derepression of an inflammatory program in these cells. The dataset consists of four sample groups: [1] 3T3-L1 preadipocytes (passage 19) transfected with a control scrambled siRNA at 24h after transfection (siC.24h), [2] 3T3-L1 preadipocytes (p.19) transfected with a siRNA directed against LSD1 at 24h after transfection (siLsd1.24h), [3] 3T3-L1 preadipocytes (p.21) transfected with a control scrambled siRNA at 48h after transfection (siC.48h), and [4] 3T3-L1 preadipocytes (p.21) transfected with a siRNA directed against LSD1 at 48h after transfection (siLsd1.48h). The 24h sample groups (siC.24h and siLsd1.24h) consist of two biological replicate samples; the 48h sample groups (siC.48h and siLsd1.48h) consist of three biological replicate samples. Each sample was hybridized to a separate array, for a total of ten arrays.

2013-12-31 | E-GEOD-25423 | biostudies-arrayexpress

Mouse interscapular brown, subscapular white and inguinal white adipose tissue

Project description:Adult mouse were kept at room temperature, RNAseq was performed for interscapular brown, subscapular white and inguinal white adipose tissue

2020-07-13 | E-MTAB-9192 | biostudies-arrayexpress

Brown Adipose Tissue

Project description:Brown Adipose Tissue

| PRJNA1046054 | ENA

RNA-seq of Brown and ingWhite adipose tissue at RT, TN and TN-HFD conditions

Project description:Mice were kept at RT, thermoneutrality (humanized condition) and thermoneutrality plus high fat diet. Inter scapular brown adipose tissue and inguinal white adipose tissue were used for RNA seq. Illumina Truseq ribosomal RNA depletion protocol was used.

2019-08-05 | E-MTAB-7561 | biostudies-arrayexpress

Expression Profiles of miRNAs in brown fat of mice at room temperature and cold exposure (8C)

Project description:microRNAs levels were measured in brown adipose tissue of male C57Bl6N mice that were kept at RT or during cold exposure (8°C) for 24 hrs. Several miRNAs including myomirs were identified to be regulated in response to cold.

2012-11-01 | GSE41306 | GEO

Systemic LSD1 inhibition prevents aberrant remodeling of metabolism in obesity

Project description:The transition from lean to obese states involves systemic metabolic remodeling that impacts insulin sensitivity, lipid partitioning, inflammation, and glycemic control. Here, we have taken a pharmacological approach to test the role of a nutrient-regulated chromatin modifier, lysine-specific demethylase (LSD1), in obesity-associated metabolic reprogramming. We show that systemic administration of an LSD1 inhibitor (GSK-LSD1) reduces food intake and body weight, ameliorates non-alcoholic fatty liver disease (NAFLD), and improves insulin sensitivity and glycemic control in mouse models of obesity. GSK-LSD1 has little effect on systemic metabolism of lean mice, suggesting LSD1 has a context-dependent role in promoting maladaptive changes in obesity. Analysis of insulin target tissues identified white adipose tissue as the major site of insulin sensitization by GSK-LSD1, where it reduces adipocyte inflammation and lipolysis. We demonstrate that GSK-LSD1 reverses NAFLD in a non-hepatocyte-autonomous manner, suggesting an indirect mechanism potentially via inhibition of adipocyte lipolysis and subsequent effects on lipid partitioning. Pair-feeding experiments further revealed that effects of GSK-LSD1 on hyperglycemia and NAFLD are not a consequence of reduced food intake and weight loss. These findings suggest that targeting LSD1 could be a strategy for treatment of obesity and its associated complications including type 2 diabetes and NAFLD.

2022-10-17 | GSE210761 | GEO

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