Murine mesenchymal cells that express elevated levels of the CDK inhibitor p16(Ink4a)in vivo are not necessarily senescent
Open accessAbstract
Age-related health decline has been attributed to the accumulation of senescent cells recognized in vivo by p16(Ink4a) expression. The pharmacological elimination of p16(Ink4a)-positive cells from the tissues of mice was shown to extend a healthy lifespan. Here, we describe a population of mesenchymal cells isolated from mice that are highly p16(INK4a)-positive are proficient in proliferation but lack other properties of cellular senescence. These data, along with earlier reports on p16(Ink4a)-positive macrophages, indicate that p16(Ink4a)-positive and senescent cell populations only partially intersect, therefore, extending the list of potential cellular targets for anti- aging therapies.
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In macrophages, p16 expression is associated with proliferation of and differentiation into the proinflammatory M1 macrophage, leading to increased IL-6 secretion.
“In macrophages, p16 expression is associated with proliferation of and differentiation into the proinflammatory M1 macrophage, 84 leading to increased IL-6 secretion.”
From The costs and benefits of senotherapeutics for human health (2022) · cites this paper as [84]
Elevated SA-β-gal activity can be found in some other cells such as activated macrophages.
“its elevated activity can be found in some other cells such as activated macrophages.48,55”
From Elimination of senescent cells by β-galactosidase-targeted prodrug attenuates inflammation and restores physical function in aged mice (2020) · cites this paper as [55]
Non-senescent macrophages may exhibit SA-β-gal positivity, and microglia can also stain positive in non-senescent contexts due to their phagocytic function and possible associated change in lysosomal numbers.
“In particular, non-senescent macrophages may exhibit SA-β-gal positivity [145,146], and microglia can also stain positive in non-senescent contexts due to their phagocytic function and the possible associated change in lysosomal numbers [147].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [146]
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References 21 · Cited by 34
- Authors
- Frescas, D., Hall, B. M., Strom, E., Virtuoso, L. P., Gupta, M., Gleiberman, A. S., Rydkina, E., Balan, V., Vujcic, S., Chernova, O. B., & Gudkov, A. V.
- Affiliations
- Buffalo Society of Natural Sciences (US)
- Roswell Park Comprehensive Cancer Center (US)
- Corresponding author
- Gudkov, Andrei V.
- Venue
- Cell Cycle
- Publisher
- Informa UK Limited
- Published
- 2017-07-24
- Volume
- 16
- Issue
- 16
- Pages
- 1526-1533
- ISSN
- 1538-4101 (ISSN-L)
- 1551-4005
- PMC
- PMC5584871
- OpenAlex
- W2652194161
- Cited by
- 34
- References
- 21
- Citations by year
- 2025: 5 · 2024: 2 · 2023: 4 · 2022: 8 · 2021: 7 · 2020: 5 · 2019: 2 · 2018: 1
- FWCI
- 1.62
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cell Cycle (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Genetics › Mesenchymal stem cell research
- Keywords
- cellular senescence, p16INK4a, mesenchymal cells, senolytics, healthy lifespan extension, anti-aging therapy, senescent cell accumulation, macrophages, cell proliferation
- MeSH terms
- Animals, Humans, Mice, Inbred C57BL, Cellular Senescence, Leukocyte Common Antigens, Cyclin-Dependent Kinase Inhibitor p16, Cell Proliferation, Mesenchymal Stem Cells
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