IL1R2 and glucocorticoid responsiveness in patients with AIED
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE4277 | GEO | 2009/04/29
SECONDARY ACCESSION(S): PRJNA94945
REPOSITORIES: GEO
Similar Datasets
Project description:Glucocorticoid responsive AIED patients demonstrate alternate splicing of IL1R2 in response to dexamethasone prior to treatment. Identification of IL1R2 as a potential target gene in AIED was determined by a microarray analysis of patients with end-stage AIED and controls with non-immunologic etiologies of hearing loss undergoing cochlear implantation. Experiment Overall Design: Patients with either end-stage AIED or controls with non-immunologic etiologies of hearing loss undergoing cochlear implantation were enrolled. All patients received pneumovax 2 weeks prior to surgery. At the time of surgery, blood was taken for PBMC isolation and autologous perilymph was harvested from a bloodless field. For each patient, 3 microarrays were performed: (1) unstimulated PBMC, (2) pneumovax stimulated PBMC, (3) autologous perilymph stimulated PBMC. All conditions were compared for the AIED and control subjects. IL1R2 was identified as induced in controls, but not AIED patients, in response to autologous perilymph. Findings were confirmed by QPCR.
2009-05-11 | E-GEOD-4277 | biostudies-arrayexpress
Project description:In order to elucidate molecular mechanisms of noise-induced hearing loss and dexamethasone therapy in the cochlea (inner ear), transcriptome of cochlear samples was analyzed after induction of hearing loss by exposure to intense noise in mice. Dexamethasone was intraperitoneally injected immediately following the noise trauma. Cochlear transcriptome was analyzed at 12h and 24h following the noise trauma and dexamethasone administration.
2016-12-03 | GSE85290 | GEO
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
Project description:Self-renewal and differentiation of spermatogonial stem cell (SSCs) are critical for sustaining spermatogenesis in adult mammals. SSC populations are highly heterogeneous and dynamic, imposing great challenges in their isolation and functional characterization. The current study aimed to generate Il1r2CreERT2/+; Rosa26mTmG/+ mice to pulse-label Il1r2-expressing cells; through lineage tracing, we discovered that IL1R2+ SSCs, essential for spermiogenesis, possess long-term capacities of self-renewal and differentiation. Under injury-induced regenerative conditions, disruption of spermatogenesis can reactivate IL1R2+ SSCs for proliferation via the PI3K-AKT-mTOR pathway to replenish the SSC pool. We further validated our discovery by systematically characterizing both mouse and human IL1R2+ SSCs isolated. Our findings confirmed the important role of IL1R2+ SSCs in the maintenance of spermatogenesis and regeneration after spermatogenic injury; IL1R2 might serve as a promising marker for enriching human and mouse SSCs.
2026-02-03 | GSE301767 | GEO
Project description:Preterm infants exhibit marked heterogeneity in the developmental stages of their immune systems at birth, which vary significantly across gestational ages. The molecular basis of immune incompetence in preterm infants and its association with immunosuppressive mechanisms have not been fully elucidated. To gain a comprehensive understanding of immune heterogeneity pertaining to the early neonatal immune system, we collected peripheral blood samples from preterm infants and full-term infants within 12 h after birth alongside peripheral blood samples from four adults for comparative single-cell transcription analysis. Using single-cell RNA sequencing, we found that myeloid-derived cells from the peripheral blood of preterm infants, especially extremely preterm infants (< 28 weeks), highly expressed IL1R2. IL1R2+ myeloid-derived cells with S100P high expression and IL1R2+ regulatory T cells with LEF1 high expression may play an important role in immunosuppression during early immune development. High expression of IL1R2 in preterm infants may lead to immune suppression, and IL1R2 may affect both myeloid-derived cells and regulatory T cells, promoting immunosuppression with high S100P and LEF1 expression and playing an important role in immune suppression during early immune development in preterm infants.
2026-07-07 | GSE301989 | GEO
Project description:The cochlea possesses a robust circadian clock machinery that regulates auditory function. How the cochlear clock is influenced by the circadian system remains unknown. Here we show that cochlear rhythms are system-driven and require local Bmal1 as well as central input from the suprachiasmatic nuclei (SCN). SCN ablations disrupted the circadian expression of the core clock genes in the cochlea. Since the circadian secretion of glucocorticoids (GCs) is controlled by the SCN and that GCs are known to modulate auditory function, we assessed their influence on circadian gene expression. Removal of circulating GCs by adrenalectomy (ADX) did not have a major impact on core clock gene expression in the cochlea. Rather it abolished the transcription of clock-controlled genes involved in inflammation. ADX abolished the known differential auditory sensitivity to day and night noise trauma and prevented the induction of GABA-ergic and glutamate receptors mRNA transcripts. However, these improvements were unrelated to changes at the synaptic level suggesting other cochlear functions may be involved. Due to this circadian regulation of noise sensitivity by GCs, we evaluated the actions of the synthetic glucocorticoid dexamethasone (DEX) at different times of the day. DEX was effective in protecting from acute noise trauma only when administered during daytime, when circulating glucocorticoids are low, indicating that chronopharmacological approaches are important for obtaining optimal treatment strategies for hearing loss. GCs appear as a major regulator of the differential sensitivity to day or night noise trauma, a mechanism likely involving the circadian control of inflammatory responses.
2019-06-15 | GSE107086 | GEO
Project description:The cochlea possesses a robust circadian clock machinery that regulates auditory function. How the cochlear clock is influenced by the circadian system remains unknown. Here we show that cochlear rhythms are system-driven and require local Bmal1 as well as central input from the suprachiasmatic nuclei (SCN). SCN ablations disrupted the circadian expression of the core clock genes in the cochlea. Since the circadian secretion of glucocorticoids (GCs) is controlled by the SCN and that GCs are known to modulate auditory function, we assessed their influence on circadian gene expression. Removal of circulating GCs by adrenalectomy (ADX) did not have a major impact on core clock gene expression in the cochlea. Rather it abolished the transcription of clock-controlled genes involved in inflammation. ADX abolished the known differential auditory sensitivity to day and night noise trauma and prevented the induction of GABA-ergic and glutamate receptors mRNA transcripts. However, these improvements were unrelated to changes at the synaptic level suggesting other cochlear functions may be involved. Due to this circadian regulation of noise sensitivity by GCs, we evaluated the actions of the synthetic glucocorticoid dexamethasone (DEX) at different times of the day. DEX was effective in protecting from acute noise trauma only when administered during daytime, when circulating glucocorticoids are low, indicating that chronopharmacological approaches are important for obtaining optimal treatment strategies for hearing loss. GCs appear as a major regulator of the differential sensitivity to day or night noise trauma, a mechanism likely involving the circadian control of inflammatory responses.
2019-06-15 | GSE88954 | GEO
Project description: Not available
| S-EPMC2670509 | biostudies-literature
Project description:In order to elucidate molecular mechanisms of noise-induced hearing loss in the cochlea (inner ear), transcriptome of the cochlear sample was analyzed after induction of hearing loss by exposure to intense noise in mice. Cochlear transcriptome was analyzed at 3 hours following the noise exposure.
2020-01-14 | GSE137817 | GEO
Project description:Background: Kawasaki disease (KD) is a multisystemic vasculitis of unknown aetiology in children. KD with coronary artery lesion is now the leading acquired heart disease in children. Peripheral blood mononuclear cells (PBMCs) play roles in KD. We identified hub genes based on RNA sequencing data and validated them in PBMCs and human umbilical vein endothelial cells (HUVECs) coculture with PBMCs. Methods: mRNA microarray of PBMCs from 12 acute KD patients and 12 healthy controls was performed to screen differentially expressed mRNAs (DE-mRNAs). We selected 20 KD patients and 20 healthy controls for validation, and established HUVECs coculture with PBMCs. Real time-PCR was finally conducted to confirm the reliability and validity of the expression level of DE-mRNAs from PBMCs and HUVECs coculture. Results: A total of 6039 DE-mRNAs were found (2267 upregulated, 3772 downregulated). Thirty hub genes were selected. KD PBMCs significantly impaired HUVECs viability and migration. IL1R2 was downregulated, FCGR1A, and CD177 mRNAs were upregulated in acute KD. IL1R2 was elevated, FCGR1A and CD177 mRNAs were downregulated in convalescence. And the real-time PCR and ELISA results showed IL1R2 was downregulated in acute KD PBMC-HUVECs co-cultures and elevated in convalescence. Conclusion: These findings may improve our understanding of PBMCs and HUVECs coculture with PBMCs in KD.
2026-03-26 | GSE325833 | GEO