Mouse Dbh-/- vs. Dbh+/+ E10.5 hearts
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE33906 | GEO | 2012/11/06
SECONDARY ACCESSION(S): PRJNA148253
REPOSITORIES: GEO
Similar Datasets
Project description:Genomic microarray analysis of adrenergic-deficient (Dbh-/-) vs. wild-type control (Dbh+/+) mouse heart expression at embryonic day 10.5 (E10.5). Four Dbh-/- and four Dbh+/+ E10.5 hearts were isolated, and RNA was extracted from each for genomic microarray analysis using Affymetrix 430A 2.0 arrays. The biological samples were collected and prepared in Dr. Ebert's laboratory at the Univ of Central Florida in Orlando, FL. The RNA samples were sent to GeneLogic (Gaithersburg, MD) for the microarray analysis.
2012-11-06 | E-GEOD-33906 | biostudies-arrayexpress
Project description:Gene expression analysis of whole heart samples obtained from CAR wild type and knockout mouse E10.5 embryos. We used the microarray to detect any gene expression changes in the E10.5 embronic heart due to the global deletion of CAR.
2019-10-15 | GSE138831 | GEO
Project description:Purpose: The goal of this study is to identify the differential cardiac chromatin accessibility between WT and cardiomyocyte conditional knockout (Chd4-CMko) hearts at E10.5 using ATAC-seq. Methods: Three hearts at E10.5 were pooled per genotype per replicate, and were then dissociated into single cells. 40,000 viable cells were taken for were lysed to isolate nuclei, which were treated with Tn5 transposase (Nextera DNA Sample Prep Kit, Illumina) to isolate DNA. Fragmented DNA was then amplified using bar-coded PCR primers and libraries were seuqenced. Results: 15736 differential peaks (2-fold change) were identified between E10.5 WT and Chd4-CMko hearts.
2024-04-18 | GSE260689 | GEO
Project description:Exaggerated airway constriction triggered by exposure to irritants such as allergen, also called hyperreactivity, is a hallmark of asthma and can be life-threatening. Aside from immune cells, vagal sensory neurons are important for airway hyperreactivity 1-4. However, the identity and signature of the downstream nodes of this adaptive circuit remains poorly understood. Here we show that Dbh+ neurons in the nucleus of the solitary tract (nTS) of the brainstem, and downstream neurons in the nucleus ambiguus (NA), are both necessary and sufficient for chronic allergen-induced airway hyperreactivity. We found that repeated exposures of mice to inhaled allergen activates nTS neurons in a mast cell-, interleukin 4 (IL-4)- and vagal nerve-dependent manner. Single-nucleus RNA-seq followed by RNAscope quantification of the nTS at baseline and following allergen challenges reveals that a Dbh+ population is preferentially activated. Ablation or chemogenetic inactivation of Dbh+ nTS neurons blunted, while chemogenetic activation promoted hyperreactivity. Viral tracing indicates that Dbh+ nTS neurons, capable of producing norepinephrine, project to the NA, and NA neurons are necessary and sufficient to relay allergen signals to postganglionic neurons that then directly drive airway constriction. Focusing on transmitters, delivery of norepinephrine antagonists to the NA blunted allergen-induced hyperreactivity. Together, these findings provide molecular, anatomical and functional definitions of key nodes of a canonical allergen response circuit. The knowledge opens the possibility of targeting neural modulation as an approach to control refractory allergen-induced airway constriction.
2024-04-15 | GSE211538 | GEO
Project description:Exaggerated airway constriction triggered by exposure to irritants such as allergen, also called hyperreactivity, is a hallmark of asthma and can be life-threatening. Aside from immune cells, vagal sensory neurons are important for airway hyperreactivity 1-4. However, the identity and signature of the downstream nodes of this adaptive circuit remains poorly understood. Here we show that Dbh+ neurons in the nucleus of the solitary tract (nTS) of the brainstem, and downstream neurons in the nucleus ambiguus (NA), are both necessary and sufficient for chronic allergen-induced airway hyperreactivity. We found that repeated exposures of mice to inhaled allergen activates nTS neurons in a mast cell-, interleukin 4 (IL-4)- and vagal nerve-dependent manner. Single-nucleus RNA-seq followed by RNAscope quantification of the nTS at baseline and following allergen challenges reveals that a Dbh+ population is preferentially activated. Ablation or chemogenetic inactivation of Dbh+ nTS neurons blunted, while chemogenetic activation promoted hyperreactivity. Viral tracing indicates that Dbh+ nTS neurons, capable of producing norepinephrine, project to the NA, and NA neurons are necessary and sufficient to relay allergen signals to postganglionic neurons that then directly drive airway constriction. Focusing on transmitters, delivery of norepinephrine antagonists to the NA blunted allergen-induced hyperreactivity. Together, these findings provide molecular, anatomical and functional definitions of key nodes of a canonical allergen response circuit. The knowledge opens the possibility of targeting neural modulation as an approach to control allergen-induced airway constriction.
2024-04-15 | GSE200003 | GEO
Project description:Transcriptional profiling of the atrioventricular canal from e10.5 mouse hearts comparing wild-type control with Tbx3 GH/N hypomorphic mutant microdissected tissue. The goal was to identify direct and indirect targets of the transcription factor Tbx3, because Tbx3 is expressed in the AVC and hypomorphs develop embryonic AV conduction block at e12.5.
2011-04-01 | GSE24122 | GEO
Project description:ATAC-seq of E10.5 WT and Chd4-CMko mouse hearts
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Project description:Investigating the impact of maternal age on heart, brain, face, and placental development by using RNA-seq to compare these tissues at E10.5 from young vs. aged females
2022-12-24 | GSE209522 | GEO
Project description:Brainstem Dbh+ Neurons Control Chronic Allergen-Induced Airway Hyperreactivity
| PRJNA822428 | ENA