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Transcriptomic response of B16-F1 melanomas to stearoyl-coA desaturase inhibitor A939572 in vivo

ABSTRACT: Transcriptomic response characterized by 3'RNA-seq of B16-F1 melanomas upon short-term treatment with stearoyl-coA desaturase inhibitor A939572 in vivo

PROVIDER: PRJEB33932 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3522040.fastq.gz	Fastqsanger.gz
	ERR3522041.fastq.gz	Fastqsanger.gz
	ERR3522042.fastq.gz	Fastqsanger.gz
	ERR3522043.fastq.gz	Fastqsanger.gz
	ERR3522044.fastq.gz	Fastqsanger.gz

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Intestinal stearoyl-CoA desaturase-inhibition improves obesity-associated metabolic disorders

Project description:Intestinal stearoyl-CoA desaturase-inhibition improves obesity-associated metabolic disorders

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Stearoyl-CoA desaturase mediated monounsaturated fatty acid availability supports humoral immunity

Project description:Immune cells can metabolize fatty acids (FAs) to generate energy. The source of different fatty acid species, and their impacts on humoral immunity remains poorly understood. Here we report that proliferating B cells require increased amount of monounsaturated fatty acids (MUFA) to maintain mitochondrial metabolism and mTOR activity, and to prevent excessive autophagy and endoplasmic reticular (ER) stress. Furthermore, B cell extrinsic Stearoyl-Coa desaturase (SCD) activity generates endogenous MUFA to support early B cell development and germinal center (GC) formation in vivo during immunization and influenza infection. Thus, SCD-mediated MUFA production is critical for humoral immunity.

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Stearoyl-CoA desaturase mediated monounsaturated fatty acid availability supports humoral immunity

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Intestinal stearoyl-CoA desaturase-inhibition improves obesity-associated metabolic disorders

Project description:Stearoyl-coenzyme A desaturase 1 (SCD1) catalyzes the rate-limiting step of de novo lipogenesis and modulates lipid homeostasis. Although numerous SCD1 inhibitors have been tested in treating metabolic disorders both in preclinical and clinic studies, the tissue-specific role of SCD1 in modulating obesity-associated metabolic disorders remains unclear. Here a novel role for intestinal SCD1 in obesity-associated metabolic disorders was uncovered. Intestinal SCD1 was found to be induced during obesity progression both in humans and mice. Intestine-specific, but not liver-specific, SCD1 deficiency reduced obesity and hepatic steatosis. A939572, a SCD1-specific inhibitor, ameliorated obesity and hepatic steatosis dependent on intestinal, but not hepatic, SCD1. Mechanistically, intestinal SCD1 deficiency impeded obesity-induced oxidative stress through its novel function of inducing metallothionein 1 (MT1) in intestinal epithelial cells. These results suggest that intestinal SCD1 could be a viable target that underlies the pharmacological effect of chemical SCD1 inhibition in the treatment of obesity-associated metabolic disorders.

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Molecular profiling of ADAM12+ MSCs in B16-OVA melanomas

Project description:This study investigates the transcriptome of ADAM12+ mesenchymal stromal cells (MSCs) in B16-OVA (MO5) melanomas

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Transcription profiling of livers from SCD1 knockout and wild type mice to elucidate the molecular basis of protection against adiposity in mice lacking of stearoyl-CoA desaturase-1 function

Project description:Stearoyl-CoA desaturase (SCD) is a central lipogenic enzyme catalyzing the synthesis of monounsaturated fatty acids, mainly oleate (C18:1) and palmitoleate (C16:1), which are components of membrane phospholipids, triglycerides, wax esters, and cholesterol esters. Several SCD isoforms (SCD1-3) exist in the mouse. Here we show that mice with a targeted disruption of the SCD1 isoform have reduced body adiposity, increased insulin sensitivity, and are resistant to diet-induced weight gain. The protection from obesity involves increased energy expenditure and increased oxygen consumption. Compared with the wild-type mice the SCD1-/- mice have increased levels of plasma ketone bodies but reduced levels of plasma insulin and leptin. In the SCD1-/- mice, the expression of several genes of lipid oxidation are up-regulated, whereas lipid synthesis genes are down-regulated. These observations suggest that a consequence of SCD1 deficiency is an activation of lipid oxidation in addition to reduced triglyceride synthesis and storage. Experiment Overall Design: RNA was isolated from livers of 10 individual 6-week-old female mice by using a standard method. Mouse genome U74A arrays were used to monitor the expression level of approximately 10,000 genes and expressed sequence tags (Affymetrix). Genes differentially expressed were identified by comparing expression levels in SCD1-/- and wild-type mice.

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Transcription profiling of livers of stearoyl-CoA desaturase 1-deficient mice to search for gene expression changes unique to SCD1-/- mice on a very low-fat, high- carbohydrate diet.

Project description:Stearoyl-CoA desaturase 1-deficient (SCD1-/-) mice have impaired monounsaturated fatty acid (MUFA) synthesis. When maintained on a very low-fat, high-carbohydrate (VLF-HC) diet, SCD1-/- mice develop severe hypercholesterolemia characterized by an increase in apolipoprotein B-containing lipoproteins and the appearance of lipoprotein-X. Additionally, high-density lipoprotein cholesterol is dramatically reduced in VLF-HC SCD1-/- mice. The concomitant presence of elevated plasma bile acids, bilirubin and aminotransferases in the VLF-HC SCD1-/- mouse are indicative of hepatic dysfunction. Supplementation of the VLF-HC diet with unsaturated fat (canola oil), but not saturated fat (coconut oil), prevents these plasma phenotypes. However, dietary oleate was not as effective as canola oil in reducing low-density lipoprotein cholesterol, signifying an additional role for dietary polyunsaturated fatty acid deficiency in the development of this phenotype. These results indicate that lack of SCD1 results in an increased requirement for dietary unsaturated fat to compensate for impaired MUFA synthesis and to prevent hypercholesterolemia and hepatic dysfunction. Experiment Overall Design: We used Affymetrix Mouse430v2.0 microarray chips to search for gene expression changes unique to the VLF-HC SCD1-/- group. These chips contain 45,101 probe sets representing over 39,000 transcripts and variants from over 34,000 mouse genes. We studied SCD1+/+ and SCD1-/- mice on chow or the VLF-HC diet, analyzing five individual livers from each subgroup for a total of twenty microarrays.

2007-11-01 | E-GEOD-3889 | biostudies-arrayexpress

Effect of chronic hypoxia and role of stearoyl-CoA desaturase 1 (SCD1) on the inflammatory response of human primary macrophages

Project description:Effect of chronic hypoxia and role of stearoyl-CoA desaturase 1 (SCD1) on the inflammatory response of human primary macrophages

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Hepatic stellate cell stearoyl co-A desaturase activates leukotrien B4 receptor 2-β-catanin cascade to promote liver tumorigenesis.

Project description:Hepatocellular carcinoma (HCC) is the 3rd most deadly malignancy. Activated hepatic stellate cells (aHSC) give rise to cancer-associated fibroblasts in HCC and are considered a potential therapeutic target. Here we report that selective ablation of stearoyl CoA desaturase-2 (Scd2) in aHSC globally suppresses nuclear CTNNB1 and YAP1 in tumors and tumor microenvironment and prevents liver tumorigenesis in male mice. Tumor suppression is associated with reduced leukotriene B4 receptor 2 (LTB4R2) and its high affinity oxylipin ligand, 12-hydroxyheptadecatrienoic acid (12-HHTrE). Genetic or pharmacological inhibition of LTB4R2, recapitulates CTNNB1 and YAP1 inactivation and tumor suppression in culture and in vivo. Single cell RNA sequencing identifies a subset of tumor-associated aHSC expressing Cyp1b1 but no other 12-HHTrE biosynthetic genes. aHSC release 12-HHTrE in a manner dependent on SCD and CYP1B1 and their conditioned medium reproduces the LTB4R2-mediated tumor-promoting effects of 12-HHTrE in HCC cells. CYP1B1-expressing aHSC are detected in proximity of LTB4R2-positive HCC cells and the growth of patient HCC organoids is blunted by LTB4R2 antagonism or knockdown. Collectively, our findings suggest aHSC-initiated 12-HHTrE-LTB4R2-CTNNB1-YAP1 pathway as a potential HCC therapeutic target.

2023-04-30 | GSE230843 | GEO

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