Deciphering Primate Retinal Aging at Single-Cell Resolution
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA454464 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7089020_1.fastq.gz | Fastqsanger.gz | |||
| SRR7089020_2.fastq.gz | Fastqsanger.gz | |||
| SRR7089030_1.fastq.gz | Fastqsanger.gz | |||
| SRR7089030_2.fastq.gz | Fastqsanger.gz | |||
| SRR7089040_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 162 |
Similar Datasets
Project description:The retina is a light-sensitive highly-organized tissue, which is vulnerable to aging and age-related retinal diseases. However, the effects of aging on retinal cell types including those present in neural retina and retinal pigment epithelium (RPE), as well as cell types in choroid layer remain largely unknown. Here, we established the single-cell transcriptomic atlas of the retina and adjacent choroid in young and aged non-human primates (NHPs), identifying 15 cell types with distinct gene expression signatures and finding several novel markers. Our analysis reveals that oxidative stress is a major aging feature of the cells in the neural retinal layer, whereas an enhanced inflammatory response is that of RPE and choroidal cells. We also found that the RPE cell is the cell type most susceptible to aging in retina, as evidenced by the decreased cell density as well as the highest numbers of differentially expressed genes overlapping with genes underlying aging and aging-related retinal diseases, along with aberrant cell-cell interactions with its two adjacent layers. Altogether, our study provides the roadmap for understanding retinal aging in a NHP model at single-cell resolution, enabling the identification of new diagnostic biomarkers and potential therapeutic targets for age-related human retinal disorders.
2020-10-20 | GSE113917 | GEO
Project description: Not available
| S-EPMC8563949 | biostudies-literature
Project description:To better understand the mechanistic basis of aging and its relationship with retinal degeneration, we examined gene expression changes in aging rod photoreceptors. Rod photoreceptor cell death is a feature of normal retinal aging and is accelerated in many retinal degenerative diseases, including AMD, the leading cause of untreatable adult blindness in the United States and other western countries. To our knowledge, the examination of age-related gene expression changes in a specific neuronal cell-type is novel, and it has allowed us to identify significant age-related changes with better resolution than is possible with whole retina samples. We used flow cytometry and a transgenic mouse with GFP-tagged rod photoreceptors to purify this specific cell population, and gene expression changes were evaluated at three time points using microarrays and quantitative RT-PCR. Our results suggest that aging is progressive, beginning even in young adult mice. Although rod photoreceptors are highly specialized neurons, our analyses revealed changes in consensus pathways of aging, including oxidative phosphorylation and stress responses affecting transcription and inflammation. In addition, we identified stress response processes that may be especially relevant for the aging retina and retinal diseases, such as angiogenesis and nuclear receptor signaling pathways that affect retinoid and lipid metabolism. We used flow cytometry and a transgenic mouse with GFP-tagged rod photoreceptors to purify this specific cell population, and gene expression changes were evaluated at three time points using microarrays and quantitative RT-PCR.
2010-06-14 | E-GEOD-22317 | biostudies-arrayexpress
Project description:Aging of the retinal pigment epithelium (RPE) leads to a gradual decline in RPE homeostasis over time, significantly impacting retinal health. Understanding the mechanisms underlying RPE aging is crucial for elucidating the background in which many age-related retinal pathologies develop. In this study, we compared the transcriptomes of young and aged mouse RPE and found a marked upregulation of immunogenic and proinflammatory genes in aging RPE. Additionally, aging RPE exhibited dysregulation of pathways associated with visual perception and extracellular matrix production. Research on aging in post-natal quiescent RPE is hindered by the absence of relevant in vitro models. We evaluated an in vitro model of chronologically aged primary human RPE to address this gap, which displayed gene expression patterns comparable to native-aged RPE. Profiling this in vitro aging model highlighted its potential utility in investigating cellular and molecular mechanisms of RPE aging and in preliminary testing of therapeutic compounds. Overall, our findings suggest chronological aging of RPE leads to the acquisition of a proinflammatory phenotype, impacting RPE function and serving as a significant factor in the development of age-related retinal pathologies.
2024-05-10 | GSE263427 | GEO
Project description:Molecular mechanisms of ovarian aging and female age-related fertility decline remain unclear. We surveyed the single-cell transcriptomic landscape of ovaries from young and aged non-human primates (NHPs) and identified seven ovarian cell types with distinct gene expression signatures, including oocyte and six types of ovarian somatic cells. In-depth dissection of gene expression dynamics of oocytes revealed four subtypes at sequential and stepwise developmental stages. Further analysis of cell type-specific aging-associated transcriptional changes uncovered the disturbance of antioxidant signaling specific to early-stage oocytes and granulosa cells, indicative of oxidative damage as a crucial factor in ovarian functional decline with age. Additionally, inactivated antioxidative pathways, increased reactive oxygen species and apoptosis were observed in granulosa cells from aged women. This study provides comprehensive understanding of the cell type-specific mechanisms underlying primate ovarian aging at single-cell resolution, revealing new diagnostic biomarkers and potential therapeutic targets for age-related human ovarian disorders.
2020-01-28 | GSE130664 | GEO
Project description:To better understand the mechanistic basis of aging and its relationship with retinal degeneration, we examined gene expression changes in aging rod photoreceptors. Rod photoreceptor cell death is a feature of normal retinal aging and is accelerated in many retinal degenerative diseases, including AMD, the leading cause of untreatable adult blindness in the United States and other western countries. To our knowledge, the examination of age-related gene expression changes in a specific neuronal cell-type is novel, and it has allowed us to identify significant age-related changes with better resolution than is possible with whole retina samples. We used flow cytometry and a transgenic mouse with GFP-tagged rod photoreceptors to purify this specific cell population, and gene expression changes were evaluated at three time points using microarrays and quantitative RT-PCR. Our results suggest that aging is progressive, beginning even in young adult mice. Although rod photoreceptors are highly specialized neurons, our analyses revealed changes in consensus pathways of aging, including oxidative phosphorylation and stress responses affecting transcription and inflammation. In addition, we identified stress response processes that may be especially relevant for the aging retina and retinal diseases, such as angiogenesis and nuclear receptor signaling pathways that affect retinoid and lipid metabolism.
2010-06-15 | GSE22317 | GEO
Project description:We used a nonhuman primate (NHP) model of ligature-induced periodontitis to identify gingival transcriptome changes associated with aging during the phases of periodontitis lesions (initiation, progression, and resolution). Four age groups of nonhuman primate were studied: Young (<3 years of age); Adolescent (3 to 7 years), Adult (12 to 15 years), and Aged (17-23 years)
2021-07-22 | GSE180588 | GEO
Project description:Single-Cell Transcriptomic Atlas of Primate Ovarian Aging
| PRJNA540933 | ENA
Project description:Deciphering human macrophage development at single-cell resolution
| PRJNA551221 | ENA
Project description:Juvenile primates develop myopia when their visual experience is degraded by lid fusion. In response to the abnormal visual input, retinal neural networks cause an excessive growth of the postequatorial segment of the eye, but the mechanism underlying this axial elongation is unknown. By combining analysis of gene expression, injection of the thymidine analog 5-bromo-2'-deoxyuridine and immunocytochemistry, we show that the retinal periphery in both juvenile rhesus macaques and green monkeys harbors a population of mitotically active neuroprogenitor cells that proliferate when the visual experience is altered by lid fusion. Furthermore, the number of dividing cells is highly correlated with the axial elongation of the eye and the resulting myopic refractive error. Thus, the retina undergoes active growth during the postnatal development of the primate eye. This growth is modulated by the visual input and accelerates considerably when the eye develops axial myopia. Keywords: disease state analysis
2006-02-27 | GSE3300 | GEO