Ontology highlight
ABSTRACT:
PROVIDER: PRJNA735022 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14727886_1.fastq.gz | Fastqsanger.gz | |||
| SRR14727886_2.fastq.gz | Fastqsanger.gz | |||
| SRR14727887_1.fastq.gz | Fastqsanger.gz | |||
| SRR14727887_2.fastq.gz | Fastqsanger.gz | |||
| SRR14727888_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:The goal of this study focues on comparing the molecular signatures of immune cells, primarily microglia, in ectopically distinct mouse models of outer retinal degeneration. These models include the sodium iodate induced RPE injury model, rhodopsin-P23H knockin mice, an advanced aging model of 2-year-old mice and young (2-month old) wild-type control mice.
2024-01-07 | GSE195891 | GEO
Project description:Sodium iodate (SI) is a commonly used model for acute retinal injury in ophthalmology research, but the single-cell transcriptional landscape across its time course remains largely unknown. Here, we establish a single-cell transcriptomic atlas for neural retinas from mice subjected to SI treatment at 0, 3, and 7 days, with 2 biological replicates per time point.
2026-06-03 | GSE312010 | GEO
Project description:Chemicals, such as MNU (N-methyl-N-nitrosourea) and NaIO3 (sodium iodate), are widely used to induce retinal degeneration in rodents. Streptozotocin (STZ) is an analog of N-acetyl glucosamine in which an MNU moiety is linked to a hexose and has a special toxic effect on insulin-producing pancreatic β-cells. It is commonly used to induce hyperglycemia to model diabetes. While intracerebroventricular injection of STZ can produce Alzheimer's disease independent of hyperglycemia, most retinal studies using STZ focus on the effects of hyperglycemia on the retina, but whether STZ has any impact on retinal cells independent of hyperglycemia is unknown. We aimed to investigate the role of cytotoxicity of STZ in rat retina. Intravitreal (5ug or 10ug) or subcutaneous (30mg/kg) injection of STZ at the early stage of newborn rats couldn’t induce hyperglycemia but caused NSIR (neonatal STZ-induced retinopathy), including reduced ERG amplitudes, retinal rosettes and apoptosis, cell cycle arrest, microglial activation, and delayed retinal angiogenesis. STZ did not affect the early-born retinal cell types but significantly reduced the late-born ones. Short-term and long-term hyperglycemia had no significant effects on the NSIR phenotypes. RNA sequencing revealed that STZ induces oxidative stress and activates the p53 pathway of retinal cells. Locally or systemically, STZ injection after P8 couldn’t induce NSIR when all retinal progenitors exit the cell cycle. Thus, NSIR in rats is independent of hyperglycemia but due to STZ’s direct cytotoxic effects on retinal progenitor cells. NSIR is a typical reaction to STZ-induced retinal oxidative stress and DNA damage. This significant finding suggests that NSIR may be a valuable model for studying retinal progenitor DNA damage-related diseases, potentially leading to new insights and treatments.
2024-07-16 | GSE272311 | GEO
Project description:Mesenchymal stem cell (MSC) heterogeneity can lead to variable treatment outcomes. Genetically modifying MSCs to express erythropoietin could confer additional therapeutic benefits that may enhance standalone MSC treatments. The goals of this study are to compare NGS-derived retinal transcriptome profiling (RNA-seq) between healthy, retinal degenerated, and stem cell-treated rat retinal degeneration models for high-throughput data analysis. MSC, Wharton's jelly Mesecnhymal stem cells; MSCEPO, EPO-expressing MSC; DPSC, dental pulp MSC stem cells Methods: Retinal mRNA profiles of 31-day-old healthy, sodium iodate-administered (retinotoxic inducer), DPSC-treated, MSC-treated, and MSCEPO-treated Sprague Dawley rats were generated by deep sequencing, in triplicate, using Illumina Nextseq 500. The sequence reads that passed quality filters were analyzed at the transcript isoform level with Salmon, and then converted to the gene level count matrices for quantification with DESeq2. The quant assay kit was used for qPCR amplification. Results: Using the Salmon-DESeq2 pipeline, we mapped about 25-35 million sequence reads per sample to the rat genome (build Rnor 6.0) and identified 20,376 transcripts in the retinas of the control and experimental groups. Approximately 500-1000 genes were found to be differentially expressed using the arbitrary cutoff of Padj<.05 and fold change>±2.0. Hierarchical clustering of differentially expressed genes revealed profiles involved in cellular regeneration,cell death, and phototransduction, which indicated the therapeutic effectiveness of the stem cells on retinal survival. Gene set enrichment analysis and pathway topology analysis showed enrichment in the aforementioned processes, Padj<.05. Conclusions: Our study represents the first detailed analysis of MSCEPO-treated retinal transcriptomes, with biologic replicates, generated by RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for further investigations in MSC enhancement methods. Our results show that NGS offers a comprehensive and more accurate quantitative and qualitative evaluation of mRNA content within the retina. We conclude that RNA-seq based retinal transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions, especially in regards to MSC-mediated tissue repair and phototransduction.
2021-04-27 | GSE164152 | GEO
Project description:We report the single base pair analysis of the ocular transcriptome from wild type and BC027072 knockout animals. Comparison was analyzed to understand gene expression changes in a mouse model for early onset retinal degeneration which phenocopies a human form of autosomal recessive retinitis pigmentosa
2015-02-03 | GSE63810 | GEO
Project description:We report the single base pair analysis of the ocular transcriptome from wild type and BC027072 knockout animals. Comparison was analyzed to understand gene expression changes in a mouse model for early onset retinal degeneration which phenocopies a human form of autosomal recessive retinitis pigmentosa Eye mRNA profiles were generated from 3 week-old C57BL/6J and BC027072 -/- in triplicate and sequenced using the Illumina HiSeq 2500
2015-02-03 | E-GEOD-63810 | biostudies-arrayexpress
Project description:Inherited retinal degenerative diseases (IRDs), including retinitis pigmentosa (RP) and Leber congenital amaurosis (LCA), cause progressive vision impairment due to photoreceptor degeneration. We previously demonstrated the protective effects of reserpine in models of CEP290-LCA and in the female Rhodopsin-P23H rat model of autosomal dominant RP. Given that reserpine is limited by side effects, we expanded our compound screen using retinal organoids from the rd16 mouse model of CEP290-LCA to include structurally diverse small molecules that may converge on proteostasis pathways. Follow-up evaluations in Rhodopsin-P23H rats, human CEP290-LCA retinal organoids, and rd10 mice (a model of PDE6B-RP) identified halofantrine as the most promising molecule, conferring strong protection on both rod and cone photoreceptors and demonstrating therapeutic potential across the divergent IRD models tested. Transcriptome analysis revealed a convergent molecular response to halofantrine across these models, primarily through upregulation of oxidative phosphorylation and ribosomal processes. Notably, halofantrine elicited significant improvements in retinal function, as assessed by electroretinography, despite pharmacokinetically limited and transient retinal exposure after subconjunctival injection in Rhodopsin-P23H rats. Our studies highlight the potential of halofantrine as a gene-independent therapy and suggest that it may be developed for ocular delivery via eye drops for the treatment of IRDs.
2026-08-06 | GSE327432 | GEO
Project description:Inherited retinal degenerative diseases (IRDs), including retinitis pigmentosa (RP) and Leber congenital amaurosis (LCA), cause progressive vision impairment due to photoreceptor degeneration. We previously demonstrated the protective effects of reserpine in models of CEP290-LCA and in the female Rhodopsin-P23H rat model of autosomal dominant RP. Given that reserpine is limited by side effects, we expanded our compound screen using retinal organoids from the rd16 mouse model of CEP290-LCA to include structurally diverse small molecules that may converge on proteostasis pathways. Follow-up evaluations in Rhodopsin-P23H rats, human CEP290-LCA retinal organoids, and rd10 mice (a model of PDE6B-RP) identified halofantrine as the most promising molecule, conferring strong protection on both rod and cone photoreceptors and demonstrating therapeutic potential across the divergent IRD models tested. Transcriptome analysis revealed a convergent molecular response to halofantrine across these models, primarily through upregulation of oxidative phosphorylation and ribosomal processes. Notably, halofantrine elicited significant improvements in retinal function, as assessed by electroretinography, despite pharmacokinetically limited and transient retinal exposure after subconjunctival injection in Rhodopsin-P23H rats. Our studies highlight the potential of halofantrine as a gene-independent therapy and suggest that it may be developed for ocular delivery via eye drops for the treatment of IRDs.
2026-08-06 | GSE327431 | GEO