Ontology highlight
ABSTRACT:
PROVIDER: PRJNA685633 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13417522_1.fastq.gz | Fastqsanger.gz | |||
| SRR13417522_2.fastq.gz | Fastqsanger.gz | |||
| SRR13417523_1.fastq.gz | Fastqsanger.gz | |||
| SRR13417523_2.fastq.gz | Fastqsanger.gz | |||
| SRR13417524_1.fastq.gz | Fastqsanger.gz |
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Project description:Gene expression profiling in 6 tissues (white adipose tissue (WAT), brown adipose tissue (BAT), cardiac muscle (CM), liver (LIV), kidney (KID), skeletal muscle (SM)) from ATGL(-/-) mice versus wildtype (ATGL+/+) mice.
2008-02-03 | E-MARS-8 | biostudies-arrayexpress
Project description:Brown adipose tissue (BAT) is known to reduce the risk of metabolic and cardiovascular diseases. Here we demonstrate that BAT transplantation alleviates pathological cardiac remodeling and reduces the incidence of heart failure post-myocardial infarction (MI). RNA-seq profile of left ventricular tissue from BAT-transplanted mice at Day3 post-MI revealed downregulation of genes associated with pro-inflammatory innate immune cells and chemokines, suggesting reduced infiltration of innate immune cells (e.g., neutrophils) into the myocardium. Concurrently, genes involved in muscle cell differentiation and cardiac repair were upregulated. These results indicate that BAT promotes post-MI cardiac repair by suppressing innate immune cell recruitment, thereby improving cardiac outcomes.
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Project description:Extracellular miRNAs are emerging as key regulators of organismal homeostasis. Here, using tissue-specific RNA labeling based on uracil phosphoribosyltransferase (UPRT)-mediated incorporation of 4-thiouracil (4TU) in male mice, we develop a roadmap of miRNA transfer from brown adipose tissue (BAT) to other tissues, where they can act to regulate energy metabolism. We demonstrate that BAT secretes miRNAs in both small extracellular vesicles (sEVs) and associated with plasma proteins, and that miRNAs in both compartments exhibit tissue-selective uptake in liver, muscle, and hypothalamus. Disruption of DICER in BAT leads to a significant depletion of multiple miRNAs in both BAT and distal tissues, including 80-90% decreases in the most abundant miRNAs in muscle. Target analyses, in vitro modeling, and PAR-CLIP analysis in muscle in vivo confirm that these BAT-secreted miRNAs directly interact with target mRNAs and alter mitochondrial function in recipient tissues. These findings provide a framework for understanding the role of BAT-secreted miRNAs in inter-organ communication.
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Project description:Specialized tissues demand support for long-term fitness. In the heart, for example, the removal of spent mitochondria by macrophages is critical for cardiac function. In an organismal-wide screening, we show here that the transfer of mitochondria to macrophages is prominent in other organs that rely on mitochondrial respiration, including the skeletal muscle and brown adipose tissue (BAT). Depletion of macrophages altered the mitochondrial activity and compromised the mechanical and thermogenic performance of these organs. Using comparative, genetic and surgical approaches, we show that the abundance of macrophages in a muscle is dictated by the mitochondrial activity of its myofibers, and that this is achieved by modulating the number of Csf1-producing fibroblasts in the tissue. Consequently, inhibition of the Csf1 receptor collapsed the mitochondrial activity of skeletal muscles. Thus, by regulating the abundance of macrophages, tissues enact an adaptive mechanism that copes with high mitochondrial turnover and supports their function.
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Project description:Objective: Brown adipose tissue (BAT) is important for thermoregulation in many mammals. Uncoupling protein 1 (UCP1) is the critical regulator of thermogenesis in BAT. Here we aimed to investigate the deacetylation control of BAT and to investigate a possible functional connection between UCP1 and sirtuin 3 (SIRT3), the master mitochondrial deacetylase.
Methods: We carried out physiological, molecular and proteomic analyses of BAT from wild-type and Sirt3KO mice when BAT is activated. Mice were either cold exposed for 2 days or were injected with the β3-adrenergic agonist, CL316,243 (1mg/kg; i.p.). Mutagenesis studies were conducted in a cellular model to assess the impact of acetyaltion lysine sites on UCP1 function. Cardiac punctures were collected for Proteomic analysis of Acylcarnitines. Isolated mitochondria were used for functional analysis of OXPHOS.
Results: Our findings showed that SIRT3 absence in mice resulted in impaired BAT lipid use, whole body thermoregulation, and respiration in BAT mitochondria, without affecting UCP1 expression. Acetylome profiling of BAT mitochondria revealed that SIRT3 regulates acetylation status of many BAT mitochondrial proteins including UCP1 and crucial upstream proteins. Mutagenesis work in cells suggested that UCP1 activity was independent of direct SIRT3-regulated lysine acetylation. However, SIRT3 impacted BAT mitochondrial activities of acylcarnitine metabolism and specific electron transport chain complexes, CI and CII.
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Project description:The activation of brown/beige adipose tissue (BAT) metabolism and the induction of uncoupling protein-1 (UCP1) expression are essential for BAT-based strategies to improve metabolic homeostasis. Adrenergic signaling is viewed as a key regulator of thermogenesis and UCP1-expression in BAT, while also operating as a potent contractile stimulator in muscle. The muscle-like gene expression patterns of UCP1+ adipocytes have previously been utilized as tissue specific markers, but have not been attributed with any functional role. Here, we demonstrate that BAT utilizes actomyosin machinery to generate tensional responses following adrenergic stimulation, similar to muscle tissues. We show that activation of actomyosin mechanics are critical for the acute induction of oxidative metabolism and uncoupled respiration in UCP1+ adipocytes. Additionally, actomyosin-mediated elasticity regulates mechanosensitive transcriptional co-activators, YAP/TAZ, that facilitate the thermogenic capacity of adipocytes. These unappreciated signaling and mechanical mechanisms may inform future strategies to promote the expansion and activation of brown/beige adipocytes.
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Project description:Cardiovascular disease remains the leading cause of death worldwide, with coronary artery disease being the primary contributor. Our recent studies suggest that activation of leptin receptors (LepRs) in the brain can improve cardiac function following myocardial infarction. However, the mechanism by which this cardioprotective effect is transmitted from the brain to the heart remains unclear. We hypothesize that brain LepR activation stimulates brown adipose tissue (BAT) to secrete extracellular vesicles (EVs) enriched with cardioprotective factors. These EVs may safeguard the heart by modulating cardiac mitochondrial function and collagen deposition. Our findings indicate that BAT ablation or BAT sympathetic denervation diminishes the cardioprotective effects of brain LepR activation. We also observed an increased concentration of EVs within BAT of rats treated with ICV leptin compared to vehicle-treated controls, an effect abolished by BAT denervation. Furthermore, knockdown of Rab27a in BAT reduced the cardioprotective benefits of brain LepR activation. MicroRNA (miR)-29c-3p was identified as a cargo of leptin-stimulated BAT-derived EVs and appears to play a key role in mitigating cardiac fibrosis after IR injury in leptin-treated animals. Thus, activation of LepR in the brain protects the heart after IR injury via sympathetic mediated BAT-derived EVs enriched with miR-29c-3p.
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