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β2-adrenergic receptor transcriptional response in HEK293 wild type, β-arrestin1/2 KO and Gαs KO cells upon isoproterenol stimulation.

ABSTRACT: β2-adrenergic receptor transcriptional response in HEK293 wild type, β-arrestin1/2 KO and Gαs KO cells upon isoproterenol stimulation.

PROVIDER: PRJNA1027499 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26372802_1.fastq.gz	Fastqsanger.gz
	SRR26372802_2.fastq.gz	Fastqsanger.gz
	SRR26372803_1.fastq.gz	Fastqsanger.gz
	SRR26372803_2.fastq.gz	Fastqsanger.gz
	SRR26372804_1.fastq.gz	Fastqsanger.gz

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β2-adrenergic receptor transcriptional response in HEK293 wild type, β-arrestin1/2 KO and Gαs KO cells upon isoproterenol stimulation.

Project description:The role of nuclear signaling by β2-adrenergic receptor (β2AR) through β-arrestins in the absence of a functional Gαs protein has not been evaluated. This has prevented a comprehensive understanding of the relative contribution of Gαs and β-arrestins to the overall β2AR signaling, thereby limiting our appreciation of how β-arrestin- or Gαs-biased ligands may affect their therapeutic outcomes. To explore the role of Gαs and β-arrestin in nuclear transcriptional programs in a global unbiased approach, we performed RNA sequencing studies in cells lacking either of these two signaling arms downstream from β2AR, followed by detailed bioinformatics analysis of gene expression signatures. We noticed multiple genes whose individual expression levels were distinct in β-arrestin1/2 and Gαs KO cells. Rather than focusing on the individual gene level, we performed a detailed analysis of gene signatures taking advantage of large datasets that were recently compiled as part of the Molecular Signatures Database (MSigDB). This approach supported that β-arrestins are not required for the activation of PKA gene signatures, including prior datasets of forskolin and CREB1 targets, while Gαs is essential. β2AR activation also led to significant changes in multiple MAPK signatures, which clearly support the activation of MAPK nuclear transcriptional programs by these receptors. Although individual variations do exist reflecting the complexities of β-arrestin- and Gαs-mediated signaling events, stimulation of these MAPK regulated gene signatures was not significantly reduced in β-arrestin1/2 KO cells but abolished in Gαs KO cells.

2023-10-17 | GSE245270 | GEO

β2-adrenergic agonists rescue lysosome acidification and function in PSEN1 deficiency by reversing defective ER to lysosome delivery of ClC-7

Project description:Lysosomal dysfunction is considered pathogenic in Alzheimer Disease (AD). Loss of Presenilin-1(PSEN1) function causing early onset AD impedes acidification via defective vATPase V0a1 subunit delivery to lysosomes. We report that isoproterenol and related β2-adrenergic agonists re-acidify lysosomes in PSEN1 KO cells and fibroblasts from PSEN1 familial AD(FAD) patients, restores lysosomal calcium homeostasis and proteolysis, and reverses impaired autophagy flux. We identify a novel rescue mechanism involving PKA-mediated facilitated delivery of ClC-7 to lysosomes, which stimulates chloride influx and reverses markedly lowered Cl- content of PSEN1 KO lysosomes. Notably, PSEN1 loss-of-function impedes ER-to-lysosome delivery of ClC-7, thus accounting for lysosomal Cl- deficits that compound pH deficits due to deficient vATPase function. Transcriptomics of PSEN1-deficient cells reveal strongly down-regulated ER-to-lysosome transport pathways and reversibility by isoproterenol. Our findings uncover a broadened PSEN1 role in lysosomal ion homeostasis and novel pH modulation of lysosomes through β-adrenergic regulation of ClC-7, which can be therapeutically modulated.

2020-02-29 | GSE136894 | GEO

β2 adrenergic receptor-mediated negative regulation of group 2 innate lymphoid cell responses

Project description:RNA sequencing of ILC2s sorted from β2 adrenergic receptor agonist-treated and non-treated mice

2018-11-27 | GSE108884 | GEO

Early gene expression in salivary gland after isoproterenol treatment

Project description:Isoproterenol, a β-adrenergic agonist, has been shown to induce salivary gland hyperplasia. To gain a better understanding of the underlying molecular changes altered by isoproterenol, microarray-based gene expression analysis was conducted on rat parotid glands at 10, 30, and 60 minutes after isoproterenol injection. After isoproterenol treatment, the number of differentially expressed genes was increased in a time-dependent manner. The regulation of up- and down-expression of genes related to cell proliferation/survival provides a better understanding of the mechanism of isoproterenol-induced parotid gland enlargement.

2015-03-01 | GSE54965 | GEO

Early gene expression in salivary gland after isoproterenol treatment

Project description:Isoproterenol, a Î²-adrenergic agonist, has been shown to induce salivary gland hyperplasia. To gain a better understanding of the underlying molecular changes altered by isoproterenol, microarray-based gene expression analysis was conducted on rat parotid glands at 10, 30, and 60 minutes after isoproterenol injection. After isoproterenol treatment, the number of differentially expressed genes was increased in a time-dependent manner. The regulation of up- and down-expression of genes related to cell proliferation/survival provides a better understanding of the mechanism of isoproterenol-induced parotid gland enlargement. For the time-course experiments, male Sprague-Dawley rats (2-3 months old) were injected intra-peritoneally with isoproterenol (20 mg/g body weight) or normal saline (control). The rats were euthanized at the indicated times and the harvested parotid glands stored at -80C until analyzed. Cells were harvested and processed at the following times: control (saline), immediately after treatment (10 min) and at 30 and 60min after treatment.

2015-03-01 | E-GEOD-54965 | biostudies-arrayexpress

Gene expression in CD8+ T-cells from tumors in Wildtype mice and β2-adrenergic receptor knockout mice

Project description:Gene profiles with NanoString in CD8+ T-cells of the non-irradiated tumors and irradiated tumors from WT and β2-AR KO mice which had been given radiation to the contralateral tumors.

2020-02-14 | GSE145262 | GEO

Isoproterenol-induced cardiac hypertrophy trigger proteome remodeling of mouse cardiomyocytes

Project description:Cardiac hypertrophy consists in the enlargement of cardiomyocytes and alteration of the extracellular matrix organization in response to physiological or pathological stress. In pathological hypertrophy ocuurs myocardial damage, loss of cardiomyocytes, fibrosis, inflammation, sarcomere disorganization and metabolic impairment, leading to cardiac dysfunction.The rodent model treated with isoproterenol induces cardiac hypertrophy due the constant activation of β-adrenergic receptors. We conducted a quantitative label-free proteomic analysis of cardiomyocytes isolated from hearts of mice treated or not with isoproterenol to better understand the molecular bases of cellular response due to isoproterenol-induced injury.

2020-05-27 | PXD013020 | Pride

Set7 deletion attenuates isoproterenol-induced cardiac fibrosis and prevents heart failure

Project description:The Set7 methyltransferase regulates the expression of several genes through the methylation of histones and modulates the activity of non-histone proteins. However, the role of Set7 in cardiac remodeling and heart failure remains unknown. To address this question, wild type (WT) and Set7 knockout (KO) male mice were injected with isoproterenol (60 mg/kg) or saline subcutaneously for 14 days. WT mice injected with isoproterenol displayed a decrease in Set7 activity in the heart, although Set7 protein levels were unchanged. WT and Set7 KO mice injected with isoproterenol exhibited an increase in the heart weight and cardiomyocyte area compared to their respective controls. However, Set7 KO mice displayed an exacerbated cardiac hypertrophy in response to isoproterenol compared to WT mice. In addition, Set7 deletion attenuated isoproterenol-induced cardiac fibrosis. Echocardiograms revealed that WT mice injected with isoproterenol had lowered ejection fractions and fractional shortening, and increased E/A ratios compared to their controls. Conversely, Set7 KO mice did not show alteration in these parameters in response to isoproterenol. Both isoproterenol and Set7 deletion changed the transcriptional profile of the heart. Moreover, Set7 deletion increased the expression of mitochondrial biogenesis and antioxidant factors in the heart and reduced the expression of cellular senescence and inflammation markers. Taken together, our data suggest that Set7 deletion reduces isoproterenol-induced myocardial fibrosis and prevents heart failure, suggesting that Set7 plays an important role in cardiac remodeling and function.

2024-04-18 | GSE207581 | GEO

β2 adrenergic receptor-mediated negative regulation of group 2 innate lymphoid cell responses

Project description:β2 adrenergic receptor-mediated negative regulation of group 2 innate lymphoid cell responses

| PRJNA429004 | ENA

Profiles of cytokines in heart after β-adrenergic stimulation in different time point

Project description:To identify the dynamic changes of cytokines in the heart upon β-adrenergic stimulation (isoproterenol, 5 mg/kg body weight) at 3hrs, 6hrs, 12hrs, 24hrs and 3days using mouse cytokine antibody arrays

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