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Cochlear fibrocyte and osteoblast lineages expressing type 2 deiodinase identified with a Dio2-CreERt2 allele

ABSTRACT: Cochlear fibrocyte and osteoblast lineages expressing type 2 deiodinase identified with a Dio2-CreERt2 allele

PROVIDER: PRJNA750482 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15288951.fastq.gz	Fastqsanger.gz
	SRR15288952.fastq.gz	Fastqsanger.gz
	SRR15288953.fastq.gz	Fastqsanger.gz
	SRR15288954.fastq.gz	Fastqsanger.gz
	SRR15288955.fastq.gz	Fastqsanger.gz

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Cochlear fibrocyte and osteoblast lineages expressing type 2 deiodinase identified with a Dio2-CreERt2 allele

Project description:Purpose: To define Dio2-expressing cochlear cell types at high resolution in juvenile mice. Methods: Individual fluorescent cells were isolated by micro-manipulator from dissociated pieces of cochlea from heterozygous Dio2ERt2 mice then used to construct single-cell RNA-seq libraries. Results: Consensus clustering of 46 cells revealed two major groups representing fibrocyte, and osteoblast lineages Conclusions: We identify Dio2-expressing fibrocyte and osteoblast lineages

2021-10-06 | GSE181057 | GEO

Transcripts identified by microarray analysis that were deregulated in E14.5 Sox2(creERT2);Tbx2(fl/fl) (Sox2-Tbx2LOF) cochlear duct.

Project description:Evaluation of transcriptional changes in the E14.5 cochlear duct epithelium upon tamoxifen-induced loss of Tbx2 in prosensory cells.

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Transcripts identified by microarray analysis that were deregulated in E14.5 Sox2(creERT2) Tbx2(fl/fl) (Sox2-Tbx2LOF) cochlear duct.

Project description:Transcripts identified by microarray analysis that were deregulated in E14.5 Sox2(creERT2) Tbx2(fl/fl) (Sox2-Tbx2LOF) cochlear duct.

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Rat Normal Cochlear Nucleus

Project description:The cochlear nucleus is the first central pathway involved in the processing of peripheral auditory activity. It is heterogeneous in neuronal populations and physiologic responses and is organized in three major subdivisions: the anterior ventral cochlear nucleus (AVCN), the posterior ventral cochlear nucleus (PVCN) and the dorsal cochlear nucleus (DCN). Although each region demonstrates multiple cell types and functions, there are predominant populations of neurons in each region that underlie the principal role each subdivision plays in auditory processing. Little is known of the underlying genetic contribution to these properties. This study sought to identify genes expressed in the subdivisions of the cochlear nucleus that may account for the anatomical and physiological characteristics of each subdivision. These data provide a genetic basis for understanding normal auditory processing in the cochlear nucleus and a template for investigating changes that may occur with hearing loss, the generation and percept of tinnitus, and central processing disorders. Keywords: normal, comparative Brown Norway rats (n=40, female, 45days) were anesthetized and decapitated. Brains were rapidly removed and the subdivisions of the cochlear nucleus (AVCN, PVCN and DCN) dissected on dry ice. Total RNA was extracted and tested for concentration and purity by spectrophotometry and integrity by gel electrophoresis. SAGE was performed using the NlaIII enzyme and Invitrogen SAGE kit. Concatemers were commercially sequenced and imported into eSAGE (Margulies and Innis, 2000) for tag extraction and frequency.

2005-12-31 | E-GEOD-3628 | biostudies-arrayexpress

Unraveling the Molecular Landscape of Lead-Induced Cochlear Synaptopathy: A Quantitative Proteomic Analysis

Project description:This study investigates how lead exposure triggers cochlear synaptopathy and hearing loss in mice. Young-adult CBA/J mice were given lead acetate in drinking water for 28 days. We assessed hearing thresholds, outer hair cell activity, and synaptic changes in the cochlea. Lead exposure raises hearing thresholds, indicating cochlear synaptopathy. Notably affects synapses in the basal turn without impacting outer hair cells. In addition to this, lead altered the abundance of 352 synaptic proteins, with the synaptic vesicle cycle pathway prominently affected. Lead-induced cochlear synaptopathy targets basal cochlear regions, implicating synaptic vesicle cycle signaling in hearing loss. Revealing specific mechanisms behind lead-induced hearing deficits enhances targeted interventions and preventive strategies, advancing our understanding of lead induced hearing loss.

2024-10-17 | PXD050415 | Pride

Transcription profiling of mouse with unilateral cochlear removal in Cochlear Nucleus at P7 and P21

Project description:Deprivation of peripheral nerve input by cochlear removal in young mice results in dramatic neuron death in the cochlear nucleus (CN). The same manipulation in older mice does not result in significant loss. The molecular basis of this critical period of vulnerability remains largely unknown. Here we identified genes regulated at early time points after cochlear removal at ages when neurons are vulnerable (postnatal day (P)7) or invulnerable (P21) to this challenge. Afferent deprivation regulated very different sets of genes at P7 and P21. These genes showed a variety of functions at both ages, but surprisingly there was no net increase in pro-apoptotic genes at P7. A large set of upregulated immune-related genes was identified at P21. Experiment Overall Design: Mice received unilateral cochlear removals. At 6, 12, 24, and 48 hours after surgery, the CN ipsilateral and contralateral were removed, and RNA isolated from separate pools of tissue for each replicate. Deafferented CN were compared to age-matched and time-matched contralateral, control CN to identify genes regulated by cochlear removal at age P7 and P21.

2008-06-13 | E-GEOD-5394 | biostudies-arrayexpress

Rat Normal Cochlear Nucleus

2006-01-01 | GSE3628 | GEO

Phosphorylation of AHR by PLK1 promotes metastasis of LUAD via DIO2-TH signaling

Project description:Metastasis of Lung adenocarcinoma (LUAD) is a major cause of death in patients. Aryl hydrocarbon receptor (AHR) is an important transcription factor involved in the initiation and progression of lung cancer. Polo-like kinase 1 (PLK1), a serine/threonine kinase, is an oncogene that promotes the malignancy of multiple cancer types. Nonetheless, the interaction between these two factors and significance in lung cancer remains to be determined. Here, we demonstrate that PLK1 phosphorylates AHR at S489 in LUAD, which leads to epithelial-mesenchymal transition (EMT) and metastatic events. RNA-seq analyses show that type 2 deiodinase (DIO2) is responsible for EMT and enhanced metastatic potential. DIO2 converts tetraiodothyronine (T4) to triiodothyronine (T3), which then activates thyroid hormone signaling. In vitro and in vivo experiments demonstrate that treatment with T3 or T4 promotes the metastasis of LUAD, whereas depletion of DIO2 or deiodinase inhibitor disrupts this property. Taken together, our results identify the phosphorylation of AHR by PLK1 as a mechanism leading to the progression of LUAD and provide possible therapeutic interventions for this event.

2023-10-22 | GSE241973 | GEO

Gene Expression after Cochlear Removal in Cochlear Nucleus at P7 and P21

Project description:Deprivation of peripheral nerve input by cochlear removal in young mice results in dramatic neuron death in the cochlear nucleus (CN). The same manipulation in older mice does not result in significant loss. The molecular basis of this critical period of vulnerability remains largely unknown. Here we identified genes regulated at early time points after cochlear removal at ages when neurons are vulnerable (postnatal day (P)7) or invulnerable (P21) to this challenge. Afferent deprivation regulated very different sets of genes at P7 and P21. These genes showed a variety of functions at both ages, but surprisingly there was no net increase in pro-apoptotic genes at P7. A large set of upregulated immune-related genes was identified at P21. Keywords: Time Course after Cochlear Removal, Age Comparison

2007-12-26 | GSE5394 | GEO

Tamoxifen timecourse in HoxA9 immortalized R26-CreERT2 Adar1fl/+ and R26-CreERT2 Adar1fl/E861A myeliod cell lines.

Project description:Tamoxifen time course in two independent R26-CreERT2 Adar1fl/+ and two independent R26-CreERT2 Adar1fl/E861A immortalised myeloid cell lines.

2024-11-21 | GSE233590 | GEO

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