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 |
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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.
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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.
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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.
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2014-10-26 | E-GEOD-56473 | biostudies-arrayexpress
Project description:Retinitis pigmentosa (RP) is a photoreceptor disease that affects approximately 100,000 people in the United States. There are currently very limited treatment options and the prognosis for most patients is progressive vision loss. Unfortunately, the understanding of the molecular underpinnings of RP initiation and progression is still poorly understood. However, the development of animal models of RP, coupled with high-throughput sequencing, has provided an opportunity to study the underlying cellular and molecular changes of this disease. Using RNA-Seq, we present the first retinal transcriptome analysis of the rd10 murine model of retinal degeneration.
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Project description:Age-related macular degeneration (AMD) is a leading cause of vision loss in the elderly, driven by retinal pigment epithelium (RPE) dysfunction, mitochondrial impairment, oxidative stress, chronic inflammation, and cellular senescence. Vutiglabridin, an orally available derivative of glabridin, has been reported to enhance mitochondrial function and mitigate metabolic stress, suggesting potential therapeutic utility in retinal aging. Here, we evaluated the efficacy and mechanism of Vutiglabridin in multiple models, including naturally aged mice representing age-associated retinal degeneration, sodium iodate (NaIO3)-induced geographic atrophy (GA), and laser-induced choroidal neovascularization (CNV). Retinal morphology and function were assessed by fundus photography, autofluorescence imaging, and electroretinography, while molecular, histological, and transcriptomic analyses were employed to investigate senescence, mitochondrial function, and inflammation. Pharmacokinetic profiling demonstrated prolonged ocular distribution of Vutiglabridin. In parallel, Paraoxonase 2 (PON2) knockdown mice were used to determine the mechanistic dependency. Vutiglabridin attenuated senescence and inflammatory markers, reduced mitochondrial ROS, and preserved retinal thickness in aged mice, while bulk RNA sequencing demonstrated partial reversal of aging-associated transcriptional signatures. In the NaIO3 model, Vutiglabridin restored mitochondrial membrane potential, enhanced mitophagy, and improved retinal function. In CNV models, it suppressed lesion growth and oxidative stress with efficacy comparable to aflibercept. Importantly, Vutiglabridin increased PON2 protein levels in vivo, and its protective effects were abolished in PON2-deficient mice, confirming a PON2-dependent mechanism. These findings establish Vutiglabridin as a promising oral therapeutic candidate for both dry and neovascular AMD, acting through PON2-mediated enhancement of mitochondrial resilience and suppression of oxidative, inflammatory, and senescent pathways.
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