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Changes in the Transcriptome of Human Astrocytes Accompanying Oxidative Stress-Induced Senescence
Open accessAbstract
Aging is a major risk factor for many neurodegenerative disorders. A key feature of aging biology that may underlie these diseases is cellular senescence. Senescent cells accumulate in tissues with age, undergo widespread changes in gene expression, and typically demonstrate altered, pro-inflammatory profiles. Astrocyte senescence has been implicated in neurodegenerative disease, and to better understand senescence-associated changes in astrocytes, we investigated changes in their transcriptome using RNA sequencing. Senescence was induced in human fetal astrocytes by transient oxidative stress. Brain-expressed genes, including those involved in neuronal development and differentiation, were downregulated in senescent astrocytes. Remarkably, several genes indicative of astrocytic responses to injury were also downregulated, including glial fibrillary acidic protein and genes involved in the processing and presentation of antigens by major histocompatibility complex class II proteins, while pro-inflammatory genes were upregulated. Overall, our findings suggest that senescence-related changes in the function of astrocytes may impact the pathogenesis of age-related brain disorders.
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“This is a hallmark of senescence in astrocytes, suggesting that these cells have taken on a secretive function [25].”
From DNA repair deficiency and senescence in concussed professional athletes involved in contact sports (2019) · cites this paper as [25]
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Metadata
- Authors
- Crowe, E. P., Tuzer, F., Gregory, B. D., Donahue, G., Gosai, S. J., Cohen, J., Leung, Y. Y., Yetkin, E., Nativio, R., Wang, L.-S., Sell, C., Bonini, N. M., Berger, S. L., Johnson, F. B., & Torres, C.
- Affiliations
- Drexel University (US)
- University of Pennsylvania (US)
- Corresponding author
- Torres, Claudio
- ORCID
- Venue
- Frontiers in Aging Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2016-08-31
- Volume
- 8
- Pages
- 208-208
- ISSN
- 1663-4365 (ISSN-L)
- PMC
- PMC5005348
- OpenAlex
- W2508551815
- Cited by
- 110
- References
- 74
- Citations by year
- 2026: 8 · 2025: 15 · 2024: 13 · 2023: 14 · 2022: 15 · 2021: 10 · 2020: 13 · 2019: 8 · 2018: 8 · 2017: 6
- FWCI
- 5.86
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Aging Neuroscience (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- ScholarlyCommons (University of Pennsylvania) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (RO1NS078283)
- National Institute on Aging (R21AG046943, F30AG043307)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- astrocyte senescence, oxidative stress, transcriptome, cellular senescence, neurodegenerative diseases, aging, pro-inflammatory genes, glial fibrillary acidic protein, MHC class II antigen presentation
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