Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The effects of terbutaline or GW9508 on TNF-alpha and IFN gamma (TNF-alpha + IFN gamma) stimulation by HaCaT

ABSTRACT: G-protein coupled receptors (GPCRs) have diverse roles in physiological processes, including immunity. Gs-coupled GPCRs increase while Gi-coupled ones decrease intracellular cAMP. Previous studies suggest that, in epithelial cells, Gs-coupled GPCRs enhance whereas Gi-coupled GPCRs suppress pro-inflammatory immune responses. In order to examine the issue, we chose beta2 adrenergic receptor and GPR40 as representatives of Gs- and Gi- coupled GPCRs, respectively, and examined their effects on TNF-alpha and IFN-gamma-(TNF-alpha + IFN-gamma) induced gene expression by HaCaT. We used microarrays to detail the global changes of gene expression induced by a beta2 adrenergic receptor agonist terbutaline or GPR40 agonist GW9508 pre-treatment in TNF-alpha + IFN-gamma - stimulated HaCaT cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE20297 | GEO | 2010/12/01

SECONDARY ACCESSION(S): PRJNA125329

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

The effects of terbutaline or GW9508 on TNF-alpha and IFN gamma (TNF-alpha + IFN gamma) stimulation by HaCaT

Project description:G-protein coupled receptors (GPCRs) have diverse roles in physiological processes, including immunity. Gs-coupled GPCRs increase while Gi-coupled ones decrease intracellular cAMP. Previous studies suggest that, in epithelial cells, Gs-coupled GPCRs enhance whereas Gi-coupled GPCRs suppress pro-inflammatory immune responses. In order to examine the issue, we chose beta2 adrenergic receptor and GPR40 as representatives of Gs- and Gi- coupled GPCRs, respectively, and examined their effects on TNF-alpha and IFN-gamma-(TNF-alpha + IFN-gamma) induced gene expression by HaCaT. We used microarrays to detail the global changes of gene expression induced by a beta2 adrenergic receptor agonist terbutaline or GPR40 agonist GW9508 pre-treatment in TNF-alpha + IFN-gamma - stimulated HaCaT cells. HaCaT cells were pre-treated with terbutaline or GW9508, TNF-alpha + IFN-gamma were then added, and cultured for another 24 h. Cells were then used for RNA extraction and hybridization on Affymetrix microarrays. We sought to clarify changes in gene expression after 1) TNF-alpha + IFN-gamma, 2) TNF-alpha + IFN-gamma + terbutaline, and 3) TNF-alpha + IFN-gamma + GW9508 treatment. To this end, we set 4 groups of samples; 1) unstimulated group, 2) TNF-alpha + IFN-gamma-stimulated group, 3) TNF-alpha + IFN-gamma + terbutaline-stimulated group, and 4) TNF-alpha + IFN-gamma + GW9508-stimulated group. In each group, HaCaT cells were stimulated in triplicate wells (n=3).

2010-12-01 | E-GEOD-20297 | biostudies-arrayexpress

Structural mechanism underlying primary and secondary coupling between GPCRs and the Gi/o family

Project description:G protein-coupled receptors (GPCRs) are the largest receptor superfamily that can propagate various extracellular stimulus into cells by coupling with heterotrimeric G proteins. G proteins are divided into four families, Gs, Gi/o, Gq/11 and G12/13, which are responsible for the transduction of discrete downstream signaling pathways. Interestingly, one receptor can couple to more than one G protein subtype with different coupling efficiency or kinetics; coupling with the highest efficiency and/or kinetics is known as ‘primary coupling’ whereas the one with lower efficiency and/or slower kinetics is known as ‘secondary coupling’. Due to its significance in human physiology, there has been a great effort to elucidate the precise mechanism of GPCR-G protein coupling, however, the complex nature of GPCR and G protein interaction raises more unanswered questions. Here, we utilized hydrogen/deuterium exchange mass spectrometry (HDX-MS) to understand the molecular mechanism underlying primary and secondary Gi/o coupling using muscarinic acetylcholine receptor type 2 (M2R) and β2-adrenergic receptor (β2AR) as the primary and secondary Gi/o-coupling receptors, respectively. Results showed the engagement of the distal C-terminus of Gi/o with the receptor differentiates primary and secondary Gi/o couplings. In addition, the interaction between the intracellular loop 2 (ICL2) of the receptor and Gi/o in primary Gi/o coupling is not as critical as in primary Gs coupling.

2020-07-02 | PXD019367 | Pride

Homo sapiens

Project description:The effects of terbutaline or GW9508 on TNF-alpha and IFN gamma (TNF-alpha + IFN gamma) stimulation by HaCaT

| PRJNA125329 | ENA

Lipolysis drives expression of the constitutively active receptor GPR3 to induce adipose thermogenesis [hBA-OE]

Project description:Thermogenic adipocytes possess a therapeutically appealing, energy-expending capacity, which is canonically cold-induced by ligand-dependent activation of b-adrenergic G protein-coupled receptors (GPCRs). Here we uncover an alternate paradigm of GPCR-mediated adipose thermogenesis through the constitutively active receptor, GPR3. We show that the N-terminus of GPR3 confers intrinsic signaling activity, resulting in continuous Gs-coupling and cAMP production without an exogenous ligand. Thus, transcriptional induction of Gpr3 represents the regulatory parallel to ligand-binding of conventional GPCRs. Consequently, increasing Gpr3 expression in thermogenic adipocytes is alone sufficient to drive energy expenditure and counteract metabolic disease in mice. Gpr3 transcription is cold-stimulated by a lipolytic signal and dietary fat potentiates GPR3-dependent thermogenesis to amplify the response to caloric excess. Moreover, we find GPR3 to be an essential, adrenergic-independent regulator of human brown adipocytes. Taken together, our findings reveal a noncanonical mechanism of GPCR control and thermogenic activation through the lipolysis-induced expression of constitutively active GPR3.

2021-04-28 | GSE173404 | GEO

Lipolysis drives expression of the constitutively active receptor GPR3 to induce adipose thermogenesis [siRNAGPR3]

2021-04-28 | GSE173389 | GEO

Lipolysis drives expression of the constitutively active receptor GPR3 to induce adipose thermogenesis [hWA]

2021-04-28 | GSE173388 | GEO

Lipolysis drives expression of the constitutively active receptor GPR3 to induce adipose thermogenesis [C-3BO]

2021-04-28 | GSE173386 | GEO

RNA-seq Analysis of Gs-linked GPCRs expressed in mouse inguinal white adipocytes (iWAT), epididymal white adipocytes (eWAT) and brown adipose tissues (BAT)

Project description:Purpose: The goals of this study are to identify Gs-linked GPCRs that are endogenously expressed by mouse adipose tissue, we subjected RNA prepared from isolated mouse adipocytes (iWAT and eWAT) and BAT tissue to RNA-seq analysis. Methods: Total RNA extracted from mature adipocytes (iWAT and eWAT) and BAT tissue of C57BL/6J mice (16-week old males) maintained on regular chow were used to construct high throughput sequencing libraries. RNAs with RIN >8 (assessed by the Agilent 2100 Bioanalyzer system) were used to prepare transcriptome libraries using the NEBNext Ultra RNA library prep kit (New England Biolabs). High throughput RNA-sequencing was performed using a HiSeq 2500 instrument (Illumina) at the NIDDK Genomic Core Facility (NIH, Bethesda, MD). Raw reads were mapped to the mouse (mm9) genome. GPCRs were extracted from the RNA-seq data using R form. Gs-coupled GPCRs were identified using the IUPHAR/BPS Guide to Pharmacology Database (https://www.guidetopharmacology.org/). Results: Our study demonstrated that mouse adipocytes/BAT tissue express several GPCRs that are selectively coupled to Gs, including the V2 vasopressin receptor, the glucagon receptor, and different melanocortin receptor subtypes.

2019-05-29 | GSE131861 | GEO

Acute effects of Salbutamol in Mouse Kidney Distal Convoluted Tubules (mpkDCT) Cells

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

Exercise-induced beta2 adrenergic receptor activation enhances the anti-leukemic activity of expanded gamma-delta T-Cells via DNAM-1 upregulation and PVR-Nectin-2 recognition

Project description:Exercise mobilizes cytotoxic lymphocytes to blood which may allow superior cell products to be manufactured for cancer therapy. Gamma-delta T-cells have shown promise for treating solid tumors, but there is a need to increase their potency against hematologic malignancies. Here, we show that human gamma-delta T-cells mobilized to blood in response to just 20-minutes of graded exercise have surface phenotypes and transcriptomic profiles associated with cytotoxicity, adhesion, migration and cytokine signaling. Following 14-days ex vivo expansion with zoledronic acid and interleukin (IL)-2, exercise mobilized gamma-delta T-cells had surface phenotypes and transcriptomic profiles associated with enhanced effector functions, and demonstrated superior cytotoxic activity against multiple hematologic tumors in vitro, and in vivo in leukemia bearing xenogeneic mice. Infusing humans with the beta1+beta2-agonist isoproterenol and administering beta1 or beta1+beta2 antagonists prior to exercise revealed these effects to be beta2-adrenergic receptor (AR) dependent. Antibody blocking of DNAM-1 on expanded gamma-delta T-cells, as well as the DNAM-1 ligands PVR and Nectin-2 on leukemic targets, abolished the enhanced anti-leukemic effects of exercise. These findings provide a mechanistic link between exercise, beta2-AR activation, and the manufacture of superior gamma-delta T-cell products for adoptive cell therapy against hematological malignancies. Expanded Vgamma9Vdelta2+ T-cells expanded, from the same participants, after both exercise (n=2) and isoproterenol infusion (n=2) underwent bulk RNA sequencing and gene expression analysis.

2024-04-04 | GSE263181 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data