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Transcriptional Roles for STAT3 in Leptin Action

ABSTRACT: Transcriptional Roles for STAT3 in Leptin Action

PROVIDER: PRJNA510419 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8333740.fastq.gz	Fastqsanger.gz
	SRR8333741.fastq.gz	Fastqsanger.gz
	SRR8333742.fastq.gz	Fastqsanger.gz
	SRR8333743.fastq.gz	Fastqsanger.gz
	SRR8333744.fastq.gz	Fastqsanger.gz

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Transcriptional Roles for STAT3 in Leptin Action

Project description:TRAP-seq from hypothalamic LepRb neurons in either control or mice lacking Stat3 in LepRb cells

2019-12-17 | GSE123983 | GEO

Defining the Transcriptional Targets of Leptin Reveals a Role for Atf3 in Leptin Action

Project description:Defining the Transcriptional Targets of Leptin Reveals a Role for Atf3 in Leptin Action

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Defining the Transcriptional Targets of Leptin Reveals a Role for Atf3 in Leptin Action

Project description:We employed translating ribosome affinity purification followed by RNA sequencing to isolate and analyze mRNA from the hypothalamic LepRb neurons of wild-type or leptin-deficient (Lepob/ob) mice treated with vehicle or exogenous leptin. Although the expression of most of the genes encoding the neuropeptides commonly considered to represent the main targets of leptin action were altered only following chronic leptin deprivation, our analysis revealed other transcripts that were coordinately regulated by leptin under multiple treatment conditions. Among these, acute leptin treatment increased expression of the transcription factor Atf3 in LepRb neurons.

2020-12-03 | GSE162603 | GEO

Leptin protects hosts cells from E. histolytica cytotoxicity via a STAT-3 dependent mechanism

Project description:Undernutrition increases susceptibility to diarrheal diseases. The adipocytokine leptin imparts protection from amebiasis. We tested the role of leptin signaling in cellular resistance to E. histolytica cytotoxicity in HEK cells transfected to express the leptin receptor. Protection from amebic killing was conferred by the leptin receptor. It required activation of the transcriptional regulator STAT3 by the leptin receptor, as mutation of the STAT3 activation domain of the receptor, or addition of a STAT3 small-molecule inhibitor, reversed protection. In contrast, a leptin receptor containing a common polymorphism (Q223R) known to increase susceptibility to amebiasis in humans provided significantly less protection. Consistent with the importance of STAT3, the Q223R polymorphism decreased l leptin-dependent STAT3 activation by 21% relative to the WT receptor (P=0.035). Microarray analysis identified potential downstream effectors of STAT3-mediated protection, most importantly TRIB1 and SOCS3, which appear to having opposing roles in the regulation of E. histolytica induced apoptosis. Together these data demonstrated that leptin increased the resistance of host cells to E. histolytica cytotoxicity via a STAT3-dependent mechanism. Additionally we found that the Q223R polymorphism in the leptin receptor, known to increase susceptibility to E. histolytica infection, decreased STAT3 activation and decreased host resistance to amebic cytotoxicity. This is the first demonstration of a host-signaling pathway that restricts amebic pathogenesis. Additionally, this finding represents an important advance in our mechanistic understanding of the role of leptin in the relationship between undernutrition and increased susceptibility to infection.

2015-01-01 | GSE35068 | GEO

Gene expression in the hypothalamus that responds to STZ-induced type 1 diabetes and can be reversed by central leptin action

Project description:Central leptin action is sufficient to restore euglycemia in type 1 diabetes via an insulin-independent manner. To examine the mechanism in the hypothalamus at the transcription level, numerous genes that showed expression changes to STZ-induced type 1 diabetes and were reversed by central leptin action were identified.

2016-02-02 | GSE72227 | GEO

Transcriptional and physiological roles for STAT proteins in leptin action.

Project description:ObjectivesLeptin acts via its receptor LepRb on specialized neurons in the brain to modulate food intake, energy expenditure, and body weight. LepRb activates signal transducers and activators of transcription (STATs, including STAT1, STAT3, and STAT5) to control gene expression.MethodsBecause STAT3 is crucial for physiologic leptin action, we used TRAP-seq to examine gene expression in LepRb neurons of mice ablated for Stat3 in LepRb neurons (Stat3LepRbKO mice), revealing the STAT3-dependent transcriptional targets of leptin. To understand roles for STAT proteins in leptin action, we also ablated STAT1 or STAT5 from LepRb neurons and expressed a constitutively-active STAT3 (CASTAT3) in LepRb neurons.ResultsWhile we also found increased Stat1 expression and STAT1-mediated transcription of leptin-regulated genes in Stat3LepRbKO mice, ablating Stat1 in LepRb neurons failed to alter energy balance (even on the Stat3LepRbKO background); ablating Stat5 in LepRb neurons also failed to alter energy balance. Importantly, expression of a constitutively-active STAT3 (CASTAT3) in LepRb neurons decreased food intake and body weight and improved metabolic parameters in leptin-deficient (ob/ob) mice, as well as in wild-type animals.ConclusionsThus, STAT3 represents the unique STAT protein required for leptin action and STAT3 suffices to mediate important components of leptin action in the absence of other LepRb signals.

| S-EPMC6437596 | biostudies-literature

Leptin stimulates cellular glycolysis through a STAT3 dependent mechanism in tilapia

Project description:Leptin stimulates cellular glycolysis through a STAT3 dependent mechanism in tilapia

| PRJNA482941 | ENA

Assessing the effect of leptin central administration on plasma proteins in insulin deficient mice.

Project description:Leptin monotherapy (i.e. without the use of administered insulin and/or any other molecule) corrects ID-induced metabolic aberrancies and promotes survival of insulin deficient rodents. These results generated great interest in the possibility of treating insulin deficient patients with leptin and/or molecule(s) underlying its beneficial effects. Hence, with the goal of identifying circulating molecule(s) underlying the advantageous effect of leptin we performed quantitative proteomic analysis of plasma and identified S100A9 as a putative peripheral mediator of leptin action. Here, to identify circulating molecule(s) underlying the advantageous effect of leptin we compared the results obtained by quantitative proteomic analysis of plasma between 2 groups of mice: streptozotocin (STZ)-treated mice that underwent intracerebroventricular (icv) leptin treatment for 12 days (STZ-Leptin) and ii) STZ-treated mice that underwent icv leptin treatment for 10 days and were withdrawn from leptin treatment for the following two days (STZ-Leptin-STOP). STZ treatment led to a massive loss of pancreatic insulin-producing β-cells, diminished pancreatic Proinsulin mRNA level, and caused severe insulinopenia, and hyperglycemia. icv leptin administration normalized hyperglycemia. However, two days after leptin delivery was halted hyperglycemia reappeared. We hypothesized that change in plasmatic protein(s) content could underlie re-emergence of hyperglycemia following decrease of leptin action.

2019-07-12 | PXD013466 | Pride

Genome Wide Binding profile and transcriptome of STAT3 and STAT3 Mutant Y640F in STAT3 Wildtype and STAT3 Mutant Y640F hematopoietic progenitor cell lines

Project description:In many human cancers the transcription factor STAT3 is constitutively active and contributes to oncogenesis, tumour growth and progression. Recently, gain-of-function mutations of STAT3 have been identified in patients suffering from various haematopoietic malignancies and are postulated to enhance the transcriptional activity of STAT3. We investigated the gene expression and binding profile of the most common STAT3 mutant Y640F compared to wild-type STAT3, describing it's mechanism of action and pinpointing to novel therapeutic intervention sites.

2023-01-25 | GSE211111 | GEO

Roles of STAT3 and STAT5 in regulation of gene expression under Th17 differentiation

Project description:Interleukin 2 (IL-2), a cytokine linked to human autoimmune diseases, limits IL-17 production. We show that deletion of Stat3 in T cells abrogates IL-17 production and attenuates autoimmunity associated with IL-2 deficiency. While STAT3 induces IL-17 and ROR?t and inhibits Foxp3, IL-2 inhibited IL-17 independently of Foxp3 and ROR?t. We found that STAT3 and STAT5 bound to multiple common sites across the Il17 genetic locus. The induction of STAT5 binding by IL-2 was associated with a reduction in STAT3 binding at these sites and the inhibition of associated active epigenetic marks. Titrating the relative activation of STAT3 and STAT5 modulated TH17 cell specification. Thus, the balance rather than the absolute magnitude of these signals determines the propensity of cells to make a key inflammatory cytokine. The roles of STAT3 and STAT5 in regulation of gene expression under Th17 differentiation was investigated. Affymetrix Mouse Genome 430 2.0 Arrays were used to evaluate global gene expression.

2011-02-09 | E-GEOD-26551 | biostudies-arrayexpress

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