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Membrane Metallo-Endopeptidase (Neprilysin) Regulates Inflammatory Response and Insulin Signaling in White Preadipocytes

ABSTRACT: Membrane Metallo-Endopeptidase (Neprilysin) Regulates Inflammatory Response and Insulin Signaling in White Preadipocytes

PROVIDER: PRJNA481868 | ENA |

REPOSITORIES: ENA

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Membrane Metallo-Endopeptidase (Neprilysin) Regulates Inflammatory Response and Insulin Signaling in White Preadipocytes (RNA-Seq)

Project description:Accumulation of subcutaneous white adipose tissue (WAT) is associated with increased insulin sensitivity, low levels of inflammation and a generally metabolically-healthy state, whereas accumulation of visceral adipose tissue is associated with insulin resistance, adipose tissue inflammation and metabolic syndrome. Membrane Metallo-Endopeptidase (MME/Neprislyin) is an extracellular, membrane-bound protease enriched in subcutaneous WAT that can target degradation of a variety of peptides, including insulin, IL6, and β-amyloids. Here, we show that MME in white preadipocytes is differently expressed in subcutaneous vs visceral WAT, and favors insulin signaling and a low inflammatory response. Thus, knockdown of MME in preadipocytes increases the inflammatory response to substance P and amyloidβ aggregates. This is associated with increased basal insulin signaling and decreased insulin-stimulated signaling. Moreover, MME differentially regulates the internalization and turnover of the α/β subunits of the insulin receptor. Thus, MME is a novel regulator of the insulin receptor in adipose tissue and may serve as a therapeutic target to increase insulin sensitivity and decrease inflammatory susceptibility.

2019-02-25 | GSE117270 | GEO

Membrane Metallo-Endopeptidase (Neprilysin) Regulates Inflammatory Response and Insulin Signaling in White Preadipocytes (Microarray Expression)

2019-02-25 | GSE117352 | GEO

Membrane Metallo-Endopeptidase (Neprilysin) Regulates Inflammatory Response and Insulin Signaling in White Preadipocytes

Project description:Accumulation of visceral white adipose tissue (WAT) associates with insulin resistance, adipose tissue inflammation, and metabolic syndrome, whereas accumulation of subcutaneous WAT may be protective. We aimed to identify molecular mechanisms that might provide mechanistic insights underlying the phenotypic differences in these tissues. Membrane Metallo-Endopeptidase (MME/Neprislyin) is an extracellular, membrane-bound protease enriched in subcutaneous WAT that can target degradation of a variety of peptides, including insulin, IL6, and β-amyloids. We hypothesized that MME contributes to adipose depot-specific metabolic properties.

2019-02-25 | GSE117353 | GEO

Membrane Metallo-Endopeptidase (Neprilysin) Regulates Inflammatory Response and Insulin Signaling in White Preadipocytes (RNA-Seq)

Project description:Membrane Metallo-Endopeptidase (Neprilysin) Regulates Inflammatory Response and Insulin Signaling in White Preadipocytes (RNA-Seq)

| PRJNA481672 | ENA

Membrane Metallo-Endopeptidase (Neprilysin) Regulates Inflammatory Response and Insulin Signaling in White Preadipocytes (Microarray Expression)

Project description:Membrane Metallo-Endopeptidase (Neprilysin) Regulates Inflammatory Response and Insulin Signaling in White Preadipocytes (Microarray Expression)

| PRJNA481870 | ENA

Membrane metallo-endopeptidase (Neprilysin) regulates inflammatory response and insulin signaling in white preadipocytes.

Project description: Not available

| S-EPMC6437599 | biostudies-literature

Expression data from preadipocytes isolated from laying hen II

Project description:Adipogenesis is one of the most intensively studied models of cellular differentiation, and transcriptional activities involved in the process have been extensively investigated. We analyzed transcripts differentially expressed between hen preadipocytes treated with adipogenic cocktail containing 500 nM dexamethasone, 0.5 mM 3-isobutyl-1-methylxanthine, 20 Âµg/mL insulin and 300 Î¼M OA (DMIOA) and non-treated control cells and transcripts differentially expressed between preadipocytes treated with DMIOA alone and those treated with a combination of DMIOA and 20(S)-hydroxycholesterol (DMIOA + 20(S)) using Affymetrix GeneChipÂ® Chicken Genome Array containing 28,000 transcripts. Preadipocytes were isolated from hen abdominal tissue, cultured and treated with DMIOA, DMIOA+Retinoic Acid

2016-05-28 | E-GEOD-81994 | 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

High fat diet-induced modifications in membrane lipid and mitochondrial-membrane protein signatures precede the development of hepatic insulin resistance in mice

Project description:In this survey we effectively combined transcriptomics, proteomics and targeted-metabolomics to analyse the temporal relationship of alterations in liver preceding and accompanying the development of HFD-mediated hepatic insulin resistance. To assess HFD-mediated alterations in physiological parameters, insulin sensitivity, and molecular adaptations in liver male C3HeB/FeJ mice treated with a high-fat diet (HFD) for 7, 14, or 21 days and compared to age- matched controls fed low-fat diet (LFD). Data indicate early systemic increases in pro-inflammatory signals, in hepatic DAG but not hepatic TAG concentrations prior to development of hepatic insulin resistance. We propose a hypothesis via which a HFD-mediated increase in the hepatic long-chain acyl-carnitine moiety in liver alters mitochondrial membrane physiology and beta-oxidation rates, thereby contributing to oxidative stress and the development of insulin resistance in liver. Alterations in the enrichment of respiratory chain complex proteins, substrate transporters, VDACs, and long-chain carnitines in mitochondrial membranes likely affect mitochondrial membrane topology, membrane dynamics (fission and fusion) and bioenergetics as well as the cross-talk between the mitochondria and other cellular compartments. In conclusion, we emphasize a tight association between HFD-induced early modifications in the organisation of mitochondrial membranes paving the road for hepatic insulin resistance.

2018-03-08 | GSE48615 | GEO

Expression data from preadipocytes isolated from laying hen

Project description:Adipogenesis is one of the most intensively studied models of cellular differentiation, and transcriptional activities involved in the process have been extensively investigated. We analyzed transcripts differentially expressed between hen preadipocytes treated with adipogenic cocktail containing 500 nM dexamethasone, 0.5 mM 3-isobutyl-1-methylxanthine, 20 ug/mL insulin and 300 uM OA (DMIOA) and non-treated control cells and transcripts differentially expressed between preadipocytes treated with DMIOA alone and those treated with a combination of DMIOA and 20(S)-hydroxycholesterol (DMIOA + 20(S)) using Affymetrix GeneChip Chicken Genome Array containing 28,000 transcripts.

2013-09-17 | GSE50880 | GEO

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