GEO accession GSE291177 is currently private and is scheduled to be released on Nov 09, 2025.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1232147 | ENA |
REPOSITORIES: ENA
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Project description:The aim of this study was to analyse the transcriptional regulation of UVB-induced ocular rosacea model on the meibomian glands of rats that overexpress the human NRC32 gene coding for mineralocorticoid receptor (P1.hMR) and age- and sex- matched wild type (WT) littlemates. 10-12 weeks old female Wild-Type (WT) and P1.hMR rats were subjected to 5-days UVB irrdiation on eyelids (UVB_WT: n = 3, UVB_P1.hMR: n = 5), together with age- and sex- matched rats without UVB-induced model (Control_WT: n = 4, Control_P1.hMR: n = 5), they were euthanized and the meibomian glands were dissected for RNA-sequencing. Total RNA samples were sequenced at the iGenSeq transcriptomic platform of the Brain and Spine Institute (ICM, Paris, France). RNA quality was checked by capillary electrophoresis and RNA integrity numbers (RIN) ranging from 8.8 to 9.3 was accepted for library generation. Quality of raw data was assessed using FastQC. Poor quality sequences and adapters were trimmed or removed with fastp, using default parameters, to retain only good quality paired reads. Illumina DRAGEN bio-IT Plateform (v3.8.4) was used for mapping on rn7 reference genome. Library orientation, library composition and coverage along transcripts were checked with Picard tools. Differential analysis has been also conducted with DESeq2. Multiple hypothesis adjusted p-values were calculated with the Benjamini-Hochberg procedure to control FDR. FDR threshold was set at 0.05, log2 fold-change threshold was set at 0.5. We identified genes differentially regulated in UVB-treated WT as compared to Control WT, and genes differentially regulated in UVB-treated P1.hMR rats as compared to Control P1.hMR.
2026-02-25 | GSE291177 | GEO
Project description:We have developed a rat model of UVB-induced ocular surface and eyelid damages mimicking ocular rosacea, a common chronic inflammatory and neurovascular ocular surface disease associated with meibomian gland dysfunction. Rat eyelids were exposed to UVB for 5 minutes daily (300mJ/cm2) for 5 days. UVB-exposed rats displayed altered meibocyte activity and lipid production, ductal epithelial hyper-keratinization, apoptosis, mitochondrial dysfunction and oxidative stress. Corneal epithelial defects, barrier disruption and abnormal innervation occurred 2 weeks after UVB exposure, subsequent to meibomian gland dysfunction. The aim of this study was to investigate the transcriptomic signature associated with meibomian gland dysfunction induced by UVB in rats. We revealed pathways related to keratinization, cell cycle and proliferation, DNA damage and repair, inflammation, immune responses, oxidative responses, and fatty acid metabolism. These regulations supported the observed functional changes of meibomian gland and were consistent with the transcriptomic signature of human meibomian gland dysfunction.
2025-12-31 | GSE277020 | GEO
Project description:We used a smooth muscle cell-specific mineralocorticoid receptor knockout mouse to generate young and aged MR-intact and SMC-MR-KO aortic miRNA to examine the effect of age on vascular miRNA alterations in the presence and absence of SMC-MR. For more information about the mouse model see: McCurley, A et al. Direct regulation of blood pressure by smooth muscle cell mineralocorticoid receptors. Nat Med. 2012 Sep;18(9):1429-33 Total miRNA was extracted from young (3-4 mo) and aged male (12mo) MR-intact and SMC-MR-KO mice to investigate aging-induced alterations in vascular miRNA expression
2016-07-29 | E-GEOD-84960 | biostudies-arrayexpress
Project description:Gene expression analysis of hearts from double transgenic mice with conditional, cardiomyocyte-specific, overexpression of the mineralocorticoid (MR) or of the glucocorticoid receptor (GR). GR-mice vs controls, MR-mice vs controls. GR: 3 sample pools hybridized to 2 microarrays each. MR: 1 sample pool hybridized to 3 microarrays. Microarray contains triplicate spots.
2010-06-18 | E-GEOD-20525 | biostudies-arrayexpress
Project description:Aldosterone, the main mineralocorticoid hormone in Humans, has a major role in maintaining the hemo-electrolytique homeostasis, by acting in the distal part of nephron. This steroid hormone mainly acts through its binding to a ligand-induced transcription factor, the mineralocorticoid receptor (MR). MR binds to specific genomic sequences, where it recruits transcriptional coregulators, to activate or repress target gene transcription. The aim of this work was to access the whole aldosterone-dependand MR target genes, by comparing sequenced data from aldosterone or vehicle-treated samples. Anti-MR ChIP-seq in Human Kidney GFP-hMR cells treated with vehicle or Aldosterone.
2015-06-12 | E-GEOD-69777 | biostudies-arrayexpress
Project description:We used a smooth muscle cell-specific mineralocorticoid receptor knockout mouse to generate young and aged MR-intact and SMC-MR-KO aortic mRNA to examine the effect of age on vascular mRNA alterations in the presence and absence of SMC-MR. For more information about the mouse model see: McCurley, A et al. Direct regulation of blood pressure by smooth muscle cell mineralocorticoid receptors. Nat Med. 2012 Sep;18(9):1429-33
2017-08-10 | GSE102397 | GEO
Project description:We used a smooth muscle cell-specific mineralocorticoid receptor knockout mouse to generate young and aged MR-intact and SMC-MR-KO aortic miRNA to examine the effect of age on vascular miRNA alterations in the presence and absence of SMC-MR. For more information about the mouse model see: McCurley, A et al. Direct regulation of blood pressure by smooth muscle cell mineralocorticoid receptors. Nat Med. 2012 Sep;18(9):1429-33
2016-07-29 | GSE84960 | GEO
Project description:Gene expression analysis of hearts from double transgenic mice with conditional, cardiomyocyte-specific, overexpression of the mineralocorticoid (MR) or of the glucocorticoid receptor (GR).
2010-06-18 | GSE20525 | GEO
Project description:Aldosterone, the main mineralocorticoid hormone in Humans, has a major role in maintaining the hemo-electrolytique homeostasis, by acting in the distal part of nephron. This steroid hormone mainly acts through its binding to a ligand-induced transcription factor, the mineralocorticoid receptor (MR). MR binds to specific genomic sequences, where it recruits transcriptional coregulators, to activate or repress target gene transcription. The aim of this work was to access the whole aldosterone-dependand MR target genes, by comparing sequenced data from aldosterone or vehicle-treated samples.
2015-06-12 | GSE69777 | GEO
Project description:Inappropriate excess of the steroid hormone aldosterone, which is a mineralocorticoid receptor (MR) agonist, is associated with increased inflammation and risk of cardiovascular disease. MR antagonists are cardioprotective and antiinflammatory in vivo, and evidence suggests that they mediate these effects in part by aldosterone- independent mechanisms. We used affymetrix to characterize the effect of Mineralocorticoid Receptor deletion on macrophage transcriptional profile, and identify its requirement in normal glucocorticoid signalling.
2010-07-30 | GSE23308 | GEO