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Diabetes induces exacerbated SARS-CoV-2 replication partly associated with ineffective pulmonary interferon responses, delayed cell-mediated immunity, and disruption of leptin receptor signaling

ABSTRACT: Diabetes induces exacerbated SARS-CoV-2 replication partly associated with ineffective pulmonary interferon responses, delayed cell-mediated immunity, and disruption of leptin receptor signaling

PROVIDER: PRJNA1128525 | ENA |

REPOSITORIES: ENA

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Diabetes induces exacerbated SARS-CoV-2 replication partly associated with ineffective pulmonary interferon responses, delayed cell-mediated immunity, and disruption of leptin receptor signaling

Project description:We evaluated the susceptibility and lung responses of type 2 diabetic and lean mice following intranasal SARS-CoV-2 infection using the mouse-adapted MA10 strain

2025-02-19 | GSE270802 | GEO

Comparison of gene expression profiles of effector T cells from leptin-receptor-deficient mice and wild type mice

Project description:We have employed whole genome microarray expression profiling as a discovery platform to identify genes differentially expressed during leptin receptor deficiency, which is partly responsible for the inhibition of T cell effector functions. Mouse CD4+CD25- T cells were purified from leptin-receptor-deficient mice and wild type mice, and stimulated with anti-CD3 and anti-CD28 for 12h. Six mice of each genotype were used. Leptin receptor deficiency-induced gene expression profiles were evaluated in mouse effector T cells from db/db mice and compared to the ones observed in their WT counterpart (db/+ mice). Two independent experiments were performed, and in each of them, 3 mice/group were pooled.

2012-09-05 | E-GEOD-29607 | biostudies-arrayexpress

Normal and ineffective erythropoiesis scRNA seq

Project description:Normal and ineffective erythropoiesis scRNA seq

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Comparison of gene expression profiles of effector T cells from leptin-receptor-deficient mice and wild type mice

2012-09-05 | GSE29607 | GEO

Leptin responsive neurons

Project description:Leptin responsive neurons

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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 microbiome

Project description:microbiome of leptin deficient mice

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Leptin responsive neurons

Project description:Genome wide association studies (GWAS) in obesity have identified a large number of noncoding loci located near genes expressed in the central nervous system. However, due to the difficulties in isolating and characterizing specific neuronal subpopulations, very few obesity-associated SNPs have been functionally characterized. Leptin responsive neurons in the hypothalamus are essential in controlling energy homeostasis and body weight. Here, we show that by combining FACS-sorting of leptin-responsive hypothalamic neuron nuclei with genomic approaches (RNA-seq, ChIP-seq, ATAC-seq), we can provide a comprehensive map of leptin-response specific regulatory elements, several of which overlap obesity-associated GWAS variants. Further demonstrating the robustness of our leptin-response neuron regulome, we functionally characterize a novel enhancer near Socs3, a leptin response-associated transcription factor. Combined, our results provide a comprehensive map of active genomic regions in leptin-responsive neurons and present a blueprint for functionally characterizing obesity-associated SNPs in the hypothalamus.

2019-04-01 | GSE112125 | GEO

Adipocyte long noncoding RNA transcriptome analysis of obese mice identified Lnc-leptin which regulates Leptin

Project description:Obesity induces profound transcriptome changes in adipocytes; recent evidence suggests that lncRNAs play key roles in this process. Here, we performed a comprehensive transcriptome study by RNA-Seq in adipocytes isolated from interscapular brown, inguinal and epididymal white adipose tissues in diet-induced obese mice. Our analysis reveals a set of obesity-dysregulated lncRNAs, many of which exhibit dynamic changes in fed vs. fasted state, potentially serving as novel molecular markers reflecting adipose energy status. Among the most prominent ones is Lnc-leptin, an lncRNA transcribed from an enhancer region upstream of Leptin. Expression of Lnc-leptin is sensitive to insulin and closely correlates to Leptin expression across diverse pathophysiological conditions. Functionally, induction of Lnc-leptin is essential for adipogenesis, and its presence is required for a loop formation between exon2 of Lnc-leptin and promoter of Leptin in mature adipocytes and the maintenance of Leptin expression in vitro and in vivo. Our study establishes Lnc-leptin as a new regulator of Leptin.

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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

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