Loss of Nfkb1 leads to early onset aging
Open accessAbstract
NF-κB is a major regulator of age-dependent gene expression and the p50/NF-κB1 subunit is an integral modulator of NF-κB signaling. Here, we examined Nfkb1-/- mice to investigate the relationship between this subunit and aging. Although Nfkb1-/- mice appear similar to littermates at six months of age, by 12 months they have a higher incidence of several observable age-related phenotypes. In addition, aged Nfkb1-/- animals have increased kyphosis, decreased cortical bone, increased brain GFAP staining and a decrease in overall lifespan compared to Nfkb1+/+. In vitro, serially passaged primary Nfkb1-/- MEFs have more senescent cells than comparable Nfkb1+/+ MEFs. Also, Nfkb1-/- MEFs have greater amounts of phospho-H2AX foci and lower levels of spontaneous apoptosis than Nfkb1+/+, findings that are mirrored in the brains of Nfkb1-/- animals compared to Nfkb1+/+. Finally, in wildtype animals a substantial decrease in p50 DNA binding is seen in aged tissue compared to young. Together, these data show that loss of Nfkb1 leads to early animal aging that is associated with reduced apoptosis and increased cellular senescence. Moreover, loss of p50 DNA binding is a prominent feature of aged mice relative to young. These findings support the strong link between the NF-κB pathway and mammalian aging.
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Nfkb1−/− mice have shortened lifespan, kyphosis, osteoporosis, tissue inflammation, and gliosis of the central nervous system.
“Nfkb1−/− mice have shortened lifespan, kyphosis, osteoporosis, tissue inflammation, and gliosis of the central nervous system.302”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [302]
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- Authors
- Bernal, G. M., Wahlstrom, J. S., Crawley, C. D., Cahill, K. E., Pytel, P., Liang, H., Kang, S., Weichselbaum, R. R., & Yamini, B.
- Affiliations
- University of Chicago (US)
- Corresponding author
- Yamini, Bakhtiar
- Venue
- Aging
- Publisher
- Impact Journals, LLC
- Published
- 2014-12-01
- Volume
- 6
- Issue
- 11
- Pages
- 931-942
- ISSN
- 1945-4589 (ISSN-L)
- PMC
- PMC4276787
- OpenAlex
- W2130156384
- Cited by
- 97
- References
- 52
- Citations by year
- 2026: 7 · 2025: 7 · 2024: 5 · 2023: 5 · 2022: 8 · 2021: 15 · 2020: 9 · 2019: 9 · 2018: 7 · 2017: 6 · 2016: 10 · 2015: 9
- FWCI
- 2.85
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by
- Locations
- Aging (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Rush University
- National Institutes of Health (UL1TR000430)
- Ludwig Center at Harvard
- National Cancer Institute (R01CA136937)
- National Center for Advancing Translational Sciences
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Keywords
- NFKB1, NF-κB signaling, p50 subunit, cellular senescence, apoptosis, kyphosis, cortical bone, lifespan, DNA damage, knockout mice, age-related phenotypes
- MeSH terms
- Age Factors, Aging, Animals, Bone and Bones, Brain, Cells, Cultured, DNA, Fibroblasts, Genotype, Gliosis, Histones, Inflammation, Kyphosis, Longevity, Mice, Inbred C57BL, Phenotype, Phosphorylation, Time Factors, Cellular Senescence, Apoptosis, Mice, Knockout, Aging, Premature, NF-kappa B p50 Subunit
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