Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1260170 | ENA |
REPOSITORIES: ENA
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Project description:Activation of the sympathetic nervous system causes pronounced metabolic changes that are mediated by multiple adrenergic receptor subtypes. Systemic treatment with β<sub>2-</sub>adrenergic receptor agonists results in multiple beneficial metabolic effects, including improved glucose homeostasis. To elucidate the underlying cellular and molecular mechanisms, we chronically treated wild-type mice and several newly developed mutant mouse strains with clenbuterol, a selective β<sub>2</sub>-adrenergic receptor agonist. Clenbuterol administration caused pronounced improvements in glucose homeostasis and prevented the metabolic deficits in mouse models of β-cell dysfunction and insulin resistance. Studies with skeletal muscle-specific mutant mice demonstrated that these metabolic improvements required activation of skeletal muscle β<sub>2</sub>-adrenergic receptors and the stimulatory G protein, G<sub>s</sub>. Unbiased transcriptomic and metabolomic analyses showed that chronic β<sub>2</sub>-adrenergic receptor stimulation caused metabolic reprogramming of skeletal muscle characterized by enhanced glucose utilization. These findings strongly suggest that agents targeting skeletal muscle metabolism by modulating β<sub>2</sub>-adrenergic receptor-dependent signaling pathways may prove beneficial as antidiabetic drugs.
2022-08-26 | MTBLS467 | MetaboLights
Project description:Analysis of the effects of 4 hr and 24 hr propranolol treatment on gene expression of SVR mouse angiosarcoma cells. The hypothesis tested in the present study was that inhibiton of beta adrenergic receptor signaling could ablate the oncogenic properties of angiosarcoma cells. Results provide important information of the response of angiosarcoma cells to ablated beta adrenergic receptor signaling. The total RNA was obtained from mouse angiosarcoma cells cultured in monolayer at 0, 4, and 24 hrs of 50 micromolar propranolol treatment. Illumina microarrays were performed to determine the whole genome expression changes following treatment.
2013-06-01 | E-GEOD-42534 | biostudies-arrayexpress
Project description:response to persistent beta 2-adrenergic receptor signaling
| PRJNA94497 | ENA
Project description:Analysis of the effects of 4 hr and 24 hr propranolol treatment on gene expression of SVR mouse angiosarcoma cells. The hypothesis tested in the present study was that inhibiton of beta adrenergic receptor signaling could ablate the oncogenic properties of angiosarcoma cells. Results provide important information of the response of angiosarcoma cells to ablated beta adrenergic receptor signaling.
2013-06-01 | GSE42534 | GEO
Project description:The sympathetic nervous system (SNS) plays a central role in blood pressure regulation. Recent studies have shown that cells of the distal convoluted tubule (DCT) can be stimulated directly via the beta-adrenergic receptor resulting in activation of the NaCl cotransporter NCC. Whether these effects are mediated by the beta1- or beta2-adrenergic receptor is unclear, and the acute signaling cascades rapidly activated by beta-adrenergic receptor stimulation in the DCT are unknown. Here in this study, we aim to identify the rapid salbutamol-mediated (beta2-adrenergic receptor) signaling in the DCT by looking at global protein phosphorylation changes in the mpkDCT cells.
2021-05-17 | PXD019051 | Pride
Project description:Myocardial aging leads to a reduction of beta-adrenergic receptor-induced metabolic and contractile responsiveness. We hypothesize that a change in the patterns of gene expression is important in these age-related events. To test this, hearts were harvested from young and aged male rats (3-4 and 20-22 mo, respectively). Total mRNA was extracted and prepared for hybridization to Affymetrix U34A GeneChips. Filtering criteria, involving fold change and a statistical significance cutoff were employed, yielding 263 probe pairs exhibiting differential signals. Of the 163 annotated genes, at least 56 (34%) were classified as signaling/cell communication. Of these 56, approximately half were directly involved in G protein-coupled receptor signaling pathways. We next determined which of these changes might be involved in anti-adrenergic activity and identified 19 potentially important gene products. Importantly, we observed a decrease in beta1-adrenergic receptor and adenylyl cyclase mRNAs, whereas the mRNA encoding beta-arrestin increased. Furthermore, the results demonstrate an increase in mRNAs encoding the adenosine A1 receptor and phospholipase D, which could increase anti-adrenergic effects. Moreover, the mRNAs encoding the muscarinic M3 receptor, nicotinic acetylcholine receptor beta3, and nicotinic acetylcholine receptor-related protein were increased as was the mRNA encoding guanylate kinase-associated protein. Interestingly, we also observed eight mRNAs whose abundance changed three- to sixfold with aging that could be considered as being compensatory. Although these results do not prove causality, they demonstrate that cardiac aging is associated with changes in the profiles of gene expression and that many of these changes may contribute to reduced adrenergic signaling.
2007-10-10 | E-GEOD-421 | biostudies-arrayexpress
Project description:In this study, we aimed to study the effect of Beta-2 Adrenergic Receptor stimulation on secreted proteins in triple negative breast cancer cell lines. We also wanted to compare protein expression in parental or bone tropic metastatic cell lines and how they respond to adrenergic signaling.
2023-07-20 | PXD030371 | Pride
Project description:In acute cold stress in mammals, JMJD1A, an H3K9 demethylase, up-regulates thermogenic gene expressions through β-adrenergic signaling in brown adipose tissue (BAT). Aside BAT-driven thermogenesis, mammals also have another mechanism to cope with long-term cold stress by inducing the browning of subcutaneous white adipose tissue (scWAT). Here, we show that this occurs through a two-step process that requires both β-adrenergic dependent phosphorylation of S265 and demethylation of H3K9me2 by JMJD1A. The histone demethylation independent acute Ucp1 induction in BAT and demethylation dependent chronic Ucp1 expression in beige-scWAT provide complementary molecular mechanisms to ensure an ordered transition between acute and chronic adaptation to cold stress. JMJD1A mediates two major signaling pathways, namlely β-adrenergic receptor and PPARγ activation, via PRDM16-PPARγ-P-JMJD1A complex for beige adipogenesis.
2018-02-16 | GSE107899 | GEO
Project description:Obesity is associated with impaired β-adrenergic receptor (Adrb1-3) signaling and lipolysis, leading to aberrant white adipose tissue (WAT) growth. WAT research has been centered on transcriptional and posttranslational regulations, but posttranscriptional regulation and mRNA modifications are poorly understood. Here, we unveil a METTL14/N6-methyladenosine (m6A) paradigm guiding β-adrenergic signaling and lipolysis. METTL14 complex installs m6A on RNA, regulating mRNA fate and translation. We found that feeding and insulin increased adipose Mettl14 and m6A levels. Adipose Mettl14 and m6A were upregulated in high fat diet (HFD)-induced obesity. Ablation of adipose Mettl14 decreased Adrb2, Adrb3, Atgl (encoding lipase), and Cig-58 (Atgl activator) transcript m6A contents while increasing their translation and protein levels, thereby enhancing adipose β-adrenergic signaling and lipolysis. Consequently, adipocyte-specific Mettl14 knockout mice were resistant to HFD-induced obesity, insulin resistance, glucose intolerance, and NAFLD. These results unravel a METTL14/m6A-based epitranscriptomic mechanism governing β-adrenergic signaling, lipolysis, and adipose growth in health and disease.
2023-06-04 | GSE233782 | GEO