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Age-related changes in the regulation of transcription factor NF-κB in rat brain
Abstract
Aging process involves an increase in stress at cellular level. We studied whether aging affects the regulation of stress responsive transcription factor NF-kappa B in brain samples of Wistar rats. Hippocampus, cerebellum, and temporal and frontal lobes of cortex were studied. We observed a significant up-regulation in the constitutive, nucleus-located NF-kappa B binding activity in 30-month-old Wistar rats compared to young and 18-month-old rats. The increase was most prominent in cerebellum and in frontal cortex, but age-related changes did not occur in hippocampus. Inducible, cytoplasmic NF-kappa B binding activity was not affected by aging in any of the samples studied. Western blot assays did not show any age-related changes in the nuclear level of p50, p52, and p65 protein components of NF-kappa B complex. Cytoplasmic level of inhibitory I kappa B-alpha was also unaffected. The increase in nuclear constitutive NF-kappa B binding activity during aging may be related to the NF-kappa B driven cellular response to adapt neurons against apoptotic pressure, as observed recently in several apoptotic conditions.
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“This morphological profile of the aged microglia first reported in rats has also been confirmed in mice, gerbils, and dogs (Hwang et al, 2008;Korhonen et al, 1997;Norden and Godbout, 2013;Streit and Xue, 2010).”
From Microglia Priming with Aging and Stress (2017) · cites this paper as Korhonen et al, 1997
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Club cell protein 16 (Cc16) deficiency increases inflamm‐aging in the lungs of mice
Laucho-Contreras, M. E., Polverino, F., Rojas, J., Wang, X., & Owen, C. A. (2018) · Physiological Reports · doi:10.14814/phy2.13797 · Cited by 25
“NF-jB is the transcription factor that is most highly associated with mammalian aging (Adler et al. 2007), and NF-jB activation is increased in most organs of old versus young rodents (Helenius et al. 1996; Korhonen et al. 1997).”
BackgroundSustained NF κB inhibition improves insulin sensitivity but is detrimental to muscle health
Zhang, N., Valentine, J. M., Zhou, Y., Li, M. E., Zhang, Y., Bhattacharya, A., Walsh, M. E., Fischer, K. E., Austad, S. N., Osmulski, P. A., et al. (2017) · Aging Cell · doi:10.1111/acel.12613 · Cited by 26
“For example, upregulation of the NFjB pathway in aged animals and older humans has been demonstrated in multiple tissues such as skeletal muscle, liver, kidney, heart, and gastric mucosa (Helenius et al., 1996; Korhonen et al., 1997; Walter & Sierra, 1998; Xiao & Majumdar, 2000; Ghosh et al., 2015).”
BackgroundFree radical-dependent changes in constitutive Nuclear factor kappa B in the aged hippocampus
Kaufmann, J. A., Bickford, P. C., & Taglialatela, G. (2002) · Neuroreport · doi:10.1097/00001756-200210280-00017 · Cited by 26
AKBULUT, K. G., Aktaş, S. H., & Akbulut, H. (2014) · Biogerontology · doi:10.1007/s10522-014-9540-1 · Cited by 25
“Although an increase in the DNA binding activity of NFjB is reported in the tissues of the aged animals, no increase in the levels of NFjB during aging has been reported (Helenius et al. 1996; Korhonen et al. 1997).”
Role of Redox Imbalance in the Molecular Mechanisms Responsible for Immunosenescence
Daynes, R. A., Enioutina, E. Y., & Jones, D. C. (2003) · Antioxidants & Redox Signaling · doi:10.1089/152308603770310185 · Cited by 27
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Mazzatti, D. J., Malavolta, M., White, A., Costarelli, L., Giacconi, R., Muti, E., Cipriano, C., Powell, J. R., & Mocchegiani, E. (2007) · Rejuvenation Research · doi:10.1089/rej.2007.0553 · Cited by 21
Hedgehog dysregulation contributes to tissue-specific inflammaging of resident macrophages
Babagana, M., Oh, K., Chakraborty, S., Pacholewska, A., Aqdas, M., & Sung, M. (2021) · Aging · doi:10.18632/aging.203422 · Cited by 20
cRel induces mitochondrial alterations in correlation with proliferation arrest
Bernard, D., Slomianny, C., Vandenbunder, B., & Abbadie, C. (2001) · Free Radical Biology and Medicine · doi:10.1016/s0891-5849(01)00668-2 · Cited by 20
Acute stress response in calorie-restricted rats to lipopolysaccharide-induced inflammation
Tsuchiya, T., Higami, Y., Komatsu, T., Tanaka, K., Honda, S., Yamaza, H., Chiba, T., Ayabe, H., & Shimokawa, I. (2005) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2004.11.007 · Cited by 20
Chronic Inflammation as an Underlying Mechanism of Ageing and Ageing-Related Diseases
Chung, K. W., Kim, D. H., Jung, H. J., Arulkumar, R., Chung, H. Y., & Yu, B. P. (2023) · Sub-cellular biochemistry/Subcellular biochemistry · doi:10.1007/978-3-031-26576-1_3 · Cited by 20
Methods to Quantify the NF-κB Pathway During Senescence
Zhang, L. J., Zhao, J., Gurkar, A. U., Niedernhofer, L. J., & Robbins, P. D. (2018) · Methods in molecular biology · doi:10.1007/978-1-4939-8931-7_18 · Cited by 20
Developmental patterns of NF-κB activation during acute hypoxia in the caudal brainstem of the rat
Simakajornboon, N., Gozal, E., & Gozal, D. (2001) · Developmental Brain Research · doi:10.1016/s0165-3806(01)00132-8 · Cited by 18
Liu, D., Wang, D., Xu, Z., Gao, J., Liu, M., Liu, Y., Jiang, M., & Zheng, D. (2015) · AGE · doi:10.1007/s11357-015-9836-3 · Cited by 17
“Moreover, NF-κB DNA binding activity is altered in the rat liver and brain and mouse macrophages with aging (Korhonen et al. 1997; Radak et al. 2004; Sarkar and Fisher 2006), indicating that NF-κB might be involved in modulating the differentially expressed miR-101b and miR-26b.”
BackgroundKitade, K., Kobayakawa, K., Saiwai, H., Matsumoto, Y., Kawaguchi, K., Iida, K., Kijima, K., Iura, H., Tamaru, T., Haruta, Y., et al. (2023) · Journal of Neurotrauma · doi:10.1089/neu.2023.0044 · Cited by 17
Systems Biology of Parkinson's Disease
Wellstead, P. E., & Cloutier, M. (2012) · Springer eBooks · doi:10.1007/978-1-4614-3411-5 · Cited by 17
Sarubbo, F., Ramis, M. R., Tejada, S., Jiménez‐García, M., Esteban, S., Miralles, A., & Moranta, D. (2023) · Journal of Functional Foods · doi:10.1016/j.jff.2023.105533 · Cited by 16
NF-κB Activation with Aging: Characterization and Therapeutic Inhibition
Zhao, J., Li, X., McGowan, S. J., Niedernhofer, L. J., & Robbins, P. D. (2015) · Methods in molecular biology · doi:10.1007/978-1-4939-2422-6_32 · Cited by 16
Metadata
- Authors
- Korhonen, P., Helenius, M., & Salminen, A.
- Affiliations
- University of Eastern Finland (FI)
- University of Jyväskylä (FI)
- Corresponding author
- Salminen, A
- ORCID
- Salminen, A
- Venue
- Neuroscience Letters
- Publisher
- Elsevier BV
- Published
- 1997-03
- Volume
- 225
- Issue
- 1
- Pages
- 61-64
- ISSN
- 0304-3940 (ISSN-L)
- OpenAlex
- W1979437866
- Cited by
- 138
- References
- 18
- Citations by year
- 2026: 2 · 2024: 2 · 2023: 6 · 2021: 3 · 2020: 7 · 2019: 2 · 2018: 7 · 2017: 4 · 2016: 4 · 2015: 6 · 2014: 4 · 2013: 8 · 2012: 12
- FWCI
- 0.56
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience Letters (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- NF-κB, brain aging, hippocampus, cerebellum, cerebral cortex, IκBα, neuronal apoptosis, stress response, Wistar rats
- MeSH terms
- Aging, Animals, Brain, Cell Nucleus, Cerebellum, Female, Frontal Lobe, Gene Expression Regulation, Hippocampus, Male, Nerve Tissue Proteins, Protein Binding, Temporal Lobe, Up-Regulation, NF-kappa B, Rats, Wistar, Rats
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