ArticleAging cell2015
Regulation of the p19(Arf)/p53 pathway by histone acetylation underlies neural stem cell behavior in senescence-prone SAMP8 mice.
Article in Aging cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Neural stem cell secretome: a secret key to unlocking the power of regeneration in the adult and aging brain.Aging brain · 2025Article
- Morphological phenotyping of the aging cochlea in inbred C57BL/6N and outbred CD1 mouse strains.Aging cell · 2025Article
- Review
- Chronic inflammation and the hallmarks of aging.Molecular metabolism · 2023Review
- Rescue of neurogenesis and age-associated cognitive decline in SAMP8 mouse: Role of transforming growth factor-alpha.Aging cell · 2023Article
- Aberrant induction of p19Arf-mediated cellular senescence contributes to neurodevelopmental defects.PLoS biology · 2022Article
- To Explore the Stem Cells Homing to GBM: The Rise to the Occasion.Biomedicines · 2022Review
- Inflammation, epigenetics, and metabolism converge to cell senescence and ageing: the regulation and intervention.Signal transduction and targeted therapy · 2021Review
- Vascular Senescence: A Potential Bridge Between Physiological Aging and Neurogenic Decline.Frontiers in neuroscience · 2021Review
- Aging and Rejuvenation of Neural Stem Cells and Their Niches.Cell stem cell · 2020Review
- Circadian glucocorticoid oscillations preserve a population of adult hippocampal neural stem cells in the aging brain.Molecular psychiatry · 2020Article
- Stem Cells of the Aging Brain.Frontiers in aging neuroscience · 2020Review
- Article
- Longitudinal Performance of Senescence Accelerated Mouse Prone-Strain 8 (SAMP8) Mice in an Olfactory-Visual Water Maze Challenge.Frontiers in behavioral neuroscience · 2018Article
- Epigenetic Regulations in Neural Stem Cells and Neurological Diseases.Stem cells international · 2018Review
- Understanding Epigenetics in the Neurodegeneration of Alzheimer's Disease: SAMP8 Mouse Model.Journal of Alzheimer's disease : JAD · 2018Review
- Epigenetic regulation in cell senescence.Journal of molecular medicine (Berlin, Germany) · 2017Review
- Protein Palmitoylation Regulates Neural Stem Cell Differentiation by Modulation of EID1 Activity.Molecular neurobiology · 2016Article
- HDAC Inhibitors as Epigenetic Regulators of the Immune System: Impacts on Cancer Therapy and Inflammatory Diseases.BioMed research international · 2016Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain aging is associated with increased neurodegeneration and reduced neurogenesis. B1/neural stem cells (B1-NSCs) of the mouse subependymal zone (SEZ) support the ongoing production of olfactory bulb interneurons, but their neurogenic potential is progressively reduced as mice age. Although age-related changes in B1-NSCs may result from increased expression of tumor suppressor proteins, accumulation of DNA damage, metabolic alterations, and microenvironmental or systemic changes, the ultimate causes remain unclear. Senescence-accelerated-prone mice (SAMP8) relative to senescence-accelerated-resistant mice (SAMR1) exhibit signs of hastened senescence and can be used as a model for the study of aging. We have found that the B1-NSC compartment is transiently expanded in young SAMP8 relative to SAMR1 mice, resulting in disturbed cytoarchitecture of the SEZ, B1-NSC hyperproliferation, and higher yields of primary neurospheres. These unusual features are, however, accompanied by premature loss of B1-NSCs. Moreover, SAMP8 neurospheres lack self-renewal and enter p53-dependent senescence after only two passages. Interestingly, in vitro senescence of SAMP8 cells could be prevented by inhibition of histone acetyltransferases and mimicked in SAMR1 cells by inhibition of histone deacetylases (HDAC). Our data indicate that expression of the tumor suppressor p19, but not of p16, is increased in SAMP8 neurospheres, as well as in SAMR1 neurospheres upon HDAC inhibition, and suggest that the SAMP8 phenotype may, at least in part, be due to changes in chromatin status. Interestingly, acute HDAC inhibition in vivo resulted in changes in the SEZ of SAMR1 mice that resembled those found in young SAMP8 mice.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.