Aging Reprograms the Rhythmic Transcriptome in the Retina
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ABSTRACT:
PROVIDER: PRJNA1281061 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR34136000_1.fastq.gz | Fastqsanger.gz | |||
| SRR34136000_2.fastq.gz | Fastqsanger.gz | |||
| SRR34136001_1.fastq.gz | Fastqsanger.gz | |||
| SRR34136001_2.fastq.gz | Fastqsanger.gz | |||
| SRR34136002_1.fastq.gz | Fastqsanger.gz |
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Project description:Aging is a significant risk factor for various retinal degenerative diseases. However, its impact on diurnal transcriptional profile of the retina remains largely unexplored. Addressing this knowledge gap is crucial given the rising prevalence of age-related retinal diseases.
2025-06-24 | GSE300500 | GEO
Project description:Mapping the daily rhythmic transcriptome in the diabetic retina
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Project description:Retinal function changes dramatically from day to night. Yet, clinical diagnosis, treatments, and experimental sampling occur during the day, leaving a significant gap in our understanding of the pathobiology occurring at night. While there is evidence that diabetes disrupts the circadian system that optimizes our physiology to the environmental light/dark cycle, the impact of such disruption is not well understood. This study investigates whether diabetes affects the retina's daily rhythm of gene expression to understand the pathobiology of diabetic retinopathy, a common complication of diabetes. Control and hyperglycemic littermate mice (Ins2Akita/J) were kept under a standard 12h:12h light/dark cycle until four months of age. Bulk mRNA sequencing was conducted in retinas collected every 4 hours throughout the 24 hr light/dark cycle. Computational approaches were used to detect rhythmicity, predict acrophase, identify differential rhythmic patterns, analyze phase set enrichment, and predict upstream regulators. The retinal transcriptome exhibited a tightly regulated rhythmic expression with a clear 12-hr axis of transcriptional rush, peaking at midday and midnight. The functions of day-peaking genes were enriched for DNA repair, RNA splicing, and ribosomal protein synthesis, whereas night-peaking genes were enriched for metabolic processes and growth factor signaling. Although the 12-hr transcriptional axis is retained in the diabetic retina, it was phase advanced by approximately 1-3 hours with a wider distribution. Upstream regulator analysis for the genes that showed phase shifts identified oxygen sensing mechanisms and HIF1alpha as regulators, but not the circadian clock, which remained in phase to the light/dark cycle. We propose a model in which early in diabetes, the diabetic retina experiences a ‘jet lag’ caused by the entrained circadian clock and its output being in one phase and metabolic pathways related to neuronal dysfunction and hypoxia driving advancement of gene expression to a different phase. Further studies are now required to evaluate the chronic implications of such internal jet lag for development of diabetic retinopathy.
2023-05-31 | GSE233440 | GEO
Project description:Objective: To determine the effects of age and topographic location on gene expression in human neural retina. Methods: Macular and peripheral neural retina RNA were isolated from human donor eyes for DNA microarray and quantitative RTPCR analyses. Results: Total RNA from human donor retina preserved integrity. Hierarchic clustering analysis demonstrates the gene expression profiles of young, old, macula and peripheral retina cluster into four distinct groups. Genes which are highly expressed in macular, peripheral, young or old retina are identified, including inhibitors of Wnt Signaling Pathway (DKK1, FZD10 and SFRP2) shown preferably expressed in the periphery. Conclusions: The transcriptome of the human retina is affected by age and topographic location. Wnt pathway inhibitors in the periphery may maintain peripheral retinal cells in an undifferentiated state. Understanding the effects of age and topographic location on gene expression may lead to the development of new therapeutic interventions for age-related eye diseases. Twleve youang and older retinal macular or prepheral RNA samples are used for DNA microarray study to compare the effects of aging and anatomic location on gene expression in human retina.
2015-05-27 | E-GEOD-32614 | biostudies-arrayexpress
Project description:Disruption of the circadian clock, which directs rhythmic expression of numerous genes, accelerates aging. To inquire how the circadian system protects organisms during aging, we compared circadian transcriptomes in heads of young and old Drosophila melanogaster. These data revealed a class of genes that adopt de novo rhythmicity during aging, termed "late life cyclers" (LLCs). We show that application of exogenous oxidative stress in young flies mimics aging by inducing robust, rhythmic LLC upregulation in a light- and CLOCK-dependent fashion. Additionally, we identified age-onset rhythmicity in some primary piRNA transcripts that overlap antisense transposable elements. To share our data, we developed a database for public viewing of graphical RNA-seq results for coding and non-coding RNAs in young and old flies. Taken together, our results suggest that aging organisms recruit the circadian system to launch a temporally coordinated defense to cope with their increasingly stressful cellular environments.
2017-01-14 | GSE81100 | GEO
Project description:This is the proteomics component of a multi-omics analysis of the aging murine retina. Age is a critical risk factor for vision-threatening retinopathies. Susceptibility to age-related retinal neurodegeneration is genetically influenced, however, no studies have addressed molecular retinal aging signatures across genetically diverse populations. Here, we profile retinal proteomics in an array of genetically diverse mice with age. Proteomics were employed to profile retinal aging signatures in C57BL/6J (B6), 129S1/SvImJ, NZO/HlLtJ (NZO), WSB/EiJ (WSB), CAST/EiJ, PWK/PhJ, NOD/ShiLtJ, A/J, and BALB/cJ mouse strains at 4, 12, and 18M. These data were collated into a publicly available resource.
2025-01-23 | PXD057861 | Pride
Project description:Background Age is the principal risk factor for neurodegeneration in both the retina and brain. The retina and brain share many biological properties; thus, insights into retinal aging and degeneration may shed light onto similar processes in the brain. Genetic makeup strongly influences susceptibility to age-related retinal disease. However, studies investigating retinal aging have not sufficiently accounted for genetic diversity. Therefore, examining molecular aging in the retina across different genetic backgrounds will enhance our understanding of human-relevant aging and degeneration in both the retina and brain—potentially improving therapeutic approaches to these debilitating conditions. Methods Transcriptomics and proteomics were employed to elucidate retinal aging signatures in nine genetically diverse mouse strains (C57BL/6J, 129S1/SvlmJ, NZO/HlLtJ, WSB/EiJ, CAST/EiJ, PWK/PhK, NOD/ShiLtJ, A/J, and BALB/cJ) across lifespan. These data predicted human disease-relevant changes in WSB and NZO strains. Accordingly, B6, WSB and NZO mice were subjected to human-relevant in vivo examinations at 4, 8, 12, and/or 18M, including: slit lamp, fundus imaging, optical coherence tomography, fluorescein angiography, and pattern/full-field electroretinography. Retinal morphology, vascular structure, and cell counts were assessed ex vivo. Results We identified common molecular aging signatures across the nine mouse strains, which included genes associated with photoreceptor function and immune activation. Genetic background strongly modulated these aging signatures. Analysis of cell type-specific marker genes predicted age-related loss of photoreceptors and retinal ganglion cells (RGCs) in WSB and NZO, respectively. Fundus exams revealed retinitis pigmentosa-relevant pigmentary abnormalities in WSB retinas and diabetic retinopathy (DR)-relevant cotton wool spots and exudates in NZO retinas. Profound photoreceptor dysfunction and loss were confirmed in WSB. Molecular analyses indicated changes in photoreceptor-specific proteins prior to loss, suggesting photoreceptor-intrinsic dysfunction in WSB. In addition, age-associated RGC dysfunction, loss, and concomitant microvascular dysfunction was observed in NZO mice. Proteomic analyses revealed an early reduction in protective antioxidant processes, which may underlie increased susceptibility to DR-relevant pathology in NZO. Conclusions Genetic context is a strong determinant of retinal aging, and our multi-omics resource can aid in understanding age-related diseases of the eye and brain. Our investigations identified and validated WSB and NZO mice as improved preclinical models relevant to common retinal neurodegenerative diseases.
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Project description:Gene expression of single cells from mouse retina during aging.
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Project description:Rod-derived Cone Viability Factor (RdCVF, alias nxnl1) is a retina-specific protein identified for its therapeutic potential in supporting cone survival during retinal degeneration. A nxnl1 knockout mouse model was created and the transcriptome used to demonstrate that the retina is compromised by the absence of nxnl1. Keywords: genetic modification, transcription-profile, retina
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Project description:Gene expression of single cells from mouse superior and inferior retina during aging.
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