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The M3 Muscarinic Acetylcholine Receptor Promotes Epidermal Differentiation

ABSTRACT: The M3 Muscarinic Acetylcholine Receptor Promotes Epidermal Differentiation

PROVIDER: PRJNA833409 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18972553.fastq.gz	Fastqsanger.gz
	SRR18972554.fastq.gz	Fastqsanger.gz
	SRR18972555.fastq.gz	Fastqsanger.gz
	SRR18972556.fastq.gz	Fastqsanger.gz
	SRR18972557.fastq.gz	Fastqsanger.gz

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The M3 Muscarinic Acetylcholine Receptor Promotes Epidermal Differentiation

Project description:The M3 muscarinic acetylcholine receptor (CHRM3) is predominantly expressed in the basal epidermal layer where it mediates the effects of the auto/paracrine cytotransmitter acetylcholine. Patients with the autoimmune blistering disease pemphigus develop autoantibodies to CHRM3 and show alterations in keratinocyte adhesion, proliferation and differentiation, suggesting that CHRM3 controls these cellular functions. Chrm3 mice display altered epidermal morphology resembling that seen in patients with pemphigus vulgaris. Here, we characterized the cellular and molecular mechanisms whereby CHRM3 controls epidermal structure and function. We used single cell (sc)RNA-seq to evaluate keratinocyte heterogeneity and identify differentially expressed genes in specific subpopulations of epidermal cells in Chrm3 KO neonatal mice.

2022-05-06 | GSE201885 | GEO

Molecular mechanism of muscarinic acetylcholine receptor M3 interaction with Gq

Project description:Muscarinic acetylcholine receptor M3 (M3) and its downstream effector Gq/11 are critical drug development targets given their involvement in numerous physiological processes and diseases. Although a cryo-electron microscopy study previously defined the structure of the M3-miniGq complex, the lack of information on the intracellular loop 3 (ICL3) of M3 and α-helical domain (AHD) of Gαq has made it difficult to comprehend the molecular mechanism of M3-Gq coupling fully. Here, we present the molecular mechanism underlying the dynamic interactions between the wild-type full-length M3 and heterotrimeric Gq using hydrogen-deuterium exchange mass spectrometry and NanoLuc Binary Technology-based cell systems. This study suggests potential binding interfaces between M3 and Gq in pre-assembled and fully active nucleotide-free complexes. In addition to well-known binding interfaces, we observed the interaction of long ICL3 with Gβγ. Furthermore, M3 ICL3 negatively affected M3-Gq coupling, and the Gαq AHD underwent unique conformational changes during M3-Gq coupling. Therefore, we propose a comprehensive molecular mechanism of M3-Gq coupling by analyzing previously well-defined binding interfaces and neglected regions, such as M3 ICL3 and the Gαq AHD.

2024-05-22 | PXD042562 | Pride

Identification of M3 muscarinic acetylcholine receptor reactive Th17 cells in patients with primary Sjögren’s syndrome

Project description:Previously M3 muscarinic acetylcholine receptore (M3R) reactive Th1 cells were identified, and here, M3R reactive Th17 cells were identified in peripheral blood of primary Sjögren’s syndrome patients using ELISpot method. To assess TCR repertoire overlap between identified M3R reactive Th17 cells, and salivary gland infiltrating T cells, we performed high throughput TCR sequencing of those cells from pSS patient.

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Identification of M3 muscarinic acetylcholine receptor reactive Th17 cells in patients with primary Sjögren’s syndrome

Project description:Identification of M3 muscarinic acetylcholine receptor reactive Th17 cells in patients with primary Sjögren’s syndrome

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whole brains from nicotinic acetylcholine receptor subunit mutant mice and littermate controls

Project description:Studies using mice with beta4 nicotinic acetylcholine receptor (nAChR) subunit deficiency (beta4-/- mice) helped reveal the roles of this subunit in bradycardiac response to vagal stimulation, nicotine-induced seizure activity and anxiety. In order to identify genes that might be related to beta4-containing nAChRs activity, we compared the mRNA expression profiles of brains from beta4-/- and wild-type mice using Affymetrix U74Avr2 microarray. Keywords: knockout mice, nicotinic acetylcholine receptor

2006-09-22 | GSE5320 | GEO

Short-term depletion of nicotinic acetylcholine receptor subunits in Drosophila enterocytes

Project description:Bulk RNAseq from whole Drosophila melanogaster guts expressing either mCherry-RNAi (control) or RNAi against nicotinic acetylcholine receptor subunits β1 and β3 (nAchRβ1 and nAchRβ3) under control of a enterocyte-specific driver to assess their role in barrier function.

2023-08-23 | GSE236069 | GEO

Neuronal Acetylcholine Couples Gonadal Gap Junction/Notch Signaling Axis to Gut Defense

Project description:Gap junctions mediate intercellular communications across cellular networks in the nervous and the immune systems, while the role in the intestinal innate immunity is poorly understood. Here, we identified that an innexin gene inx-14 encoding one of heterotypic and heteromeric gap junction subunits acts in the gonad to attenuate the intestinal defense through PMK-1/p38 pathway. The RNA-seq analyses revealed that GLP-1/Notch signaling was downregulated, while lysosome, and PMK-1/p38 MAPK signalings were upregulated by the germline-specific inx-14 RNAi in C. elegans. Loss function of either inx-14, or glp-1 exhibited enhanced resistance to PA14 infection and upregulated lysosome and PMK-1/p38 signalings. Additionally, inx-14 knockdown by germline specific RNAi upregulated muscarinic acetylcholine receptor (mAChR) genes gar-1/gar-2/gar-3. We further revealed that acetylcholine mAChR GAR-2/GAR-3 signaling functions in the intestine and downstream of lysosome signaling but upstream of PMK-1/p38 pathway to facilitate the intestinal defense. Our findings reveal a novel role for gonadal gap junction/INX-14 in host intestinal defense against pathogens and expand our understanding the functions of reproductive system in the host intestinal defense.

2023-11-01 | GSE216879 | GEO

Regulatory function of sympathetic innervation on the endo/lysosomal trafficking of acetylcholine receptor

Project description:Regulation of membrane receptors involves management of endocytosis. At the neuromuscular junction, the synapse between skeletal muscle and motoneuron, proper density of the major receptor, the acetylcholine receptor, is of utmost importance for sustaining life in context of mobility. Recent work has revealed innervation of NMJs by sympathetic neurons and destruction of them had morphological and functional consequences, suggesting influence on endocytosis. To investigate the pathways and proteins that are relevant for acetylcholine receptor turnover and affected by sympathetic signaling, proteomes of mouse hindlimb muscles from sympathectomized and saline-treated control muscles were compared. Using proteomic, Western blot, and immunofluorescence analysis in chemically sympathectomized mouse hindlimb muscles, the cause of these consequences were aimed to analyzed. This revealed extensive regulation of the proteome by the sympathetic nervous system and a possible regulatory function of the endo/lysosomal and autophagic pathway by sympathetic neuronal input. This finding might provide a new explanation to the observed benefit of sympathicomimetic treatment in several congenital myasthenic syndromes.

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RNA sequencing data describing transcriptional changes in aorta of ApoE-/- mice after alpha 7 nicotinic acetylcholine receptor (α7nAChR) stimulation.

Project description:This manuscript is a companion paper to Ulleryd M.U. et al (1). Data shown here include RNA sequencing data from whole aorta of ApoE-/- mice treated with the alpha 7 nicotinic acetylcholine receptor (α7nAChR) agonist AZ6983 for 8 weeks using subcutaneously implanted osmotic minipumps. 1. Ulleryd MA, Mjornstedt F, Panagaki D, Yang LJ, Engevall K, Gutierrez S, et al. Stimulation of alpha 7 nicotinic acetylcholine receptor (α7nAChR) inhibits atherosclerosis via immunomodulatory effects on myeloid cells Re-submitted. 2019.

2019-10-29 | GSE131162 | GEO

Transcription profiling of rat heart tissue from animals aged 4 and 22 months

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

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