Atypical pathways of NF-κB activation and aging

Kriete, Andres; Mayo, Kelli L.

doi:10.1016/j.exger.2008.12.005

Cited by 77 publications

(62 citation statements)

References 80 publications

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“…8,9 In our current study, activation of NF-κB by S. aureus in human osteoblasts has been demonstrated by two different methods. First, our immunoblot experiments demonstrated that degradation of cytoplasmic IκBa in S. aureus-infected human osteoblasts occurred in a time and dose-dependent manner ( Figures 1A and 2A).…”

Section: Discussionmentioning

confidence: 99%

“…8 Different stimuli can induce the phosphorylation of IκBa, and its subsequent ubiquitination and degradation. 9 Freed NF-κB can translocate into the nucleus, leading to the transcriptional activation of NF-κB-dependent genes, 10 such as chemokines and cytokines genes. 11 Previous studies have demonstrated that NF-κB in eukaryocyte could be activated by diverse bacteria, such as Porphyromonas gingivalis, 12 Streptococcus pyogenes, 13,14 or Mycobacterium bovis Bacillus Calmette-Guerin (BCG).…”

Section: Introductionmentioning

confidence: 99%

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Staphylococcus aureus regulates secretion of interleukin-6 and monocyte chemoattractant protein-1 through activation of nuclear factor kappaB signaling pathway in human osteoblasts

Ning¹,

Zhang²,

Guo³

et al. 2011

Braz J Infect Dis

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Objective: Activation of nuclear factor kappaB by diverse bacteria regulates the secretion of chemokines and cytokines. Staphylococcus aureus (S. aureus)-infected osteoblasts can significantly increase the secretion of interleukin-6 and monocyte chemoattractant protein-1. The aim of this study was to investigate whether S. aureus can activate nuclear factor kappaB in human osteoblasts, and whether the activation of nuclear factor kappaB by S. aureus regulates the secretion of interleukin-6 and monocyte chemoattractant protein-1. Methods: Immunoblot and electrophoretic mobility shift assay were used to detect the degradation of IκBa and activation of nuclear factor kappaB in human osteoblasts in response to S. aureus, respectively. Enzyme-linked immunosorbent assay was used to measure the secretion of interleukin-6 and monocyte chemoattractant protein-1 in the supernatants. Lastly, carbobenzoxyl-l-leucinyl-l-leucinyl-l-leucinal, an inhibitor of the nuclear factor kappaB, was used to determine if activation of nuclear factor kappaB by S. aureus in human osteoblasts regulates the secretions of interleukin-6 and monocyte chemoattractant protein-1. Results: Our results for the first time demonstrated that S. aureus can induce the degradation of IκBa and activation of nuclear factor kappaB in human osteoblasts in a time and dose-dependent manner. In addition, inhibition of nuclear factor kappaB by carbobenzoxyl-l-leucinyl-l-leucinyl-l-leucinal suppressed the secretion of interleukin-6 and monocyte chemoattractant protein-1 in the supernatants of S. aureus-infected human osteoblasts in a dose-dependent manner. Conclusions: These findings suggest that S. aureus can activate nuclear factor kappaB in human osteoblasts, and subsequently regulate the secretion of interleukin-6 and monocyte chemoattractant protein-1. The nuclear factor kappaB transcription factor regulates a number of genes involved in a wide variety of biological processes. Further study of the effects of nuclear factor kappaB activation on S. aureus-infected human osteoblast may provide us new insights into discovery of the immune mechanisms in osteomyelitis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Staphylococcus aureus regulates secretion of interleukin-6 and monocyte chemoattractant protein-1 through activation of nuclear factor kappaB signaling pathway in human osteoblasts

Ning¹,

Zhang²,

Guo³

et al. 2011

Braz J Infect Dis

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“…The NF-κB pathway plays a critical role in the inhibition of apoptosis and autophagy, which may provoke inflammatory responses during the aging process because of the accumulation of waste products in cells and thus promote the senescent phenotype. 42,43 It has been suggested that the decreased insulin/ IGF-1 signaling activates FOXO factors and extends life span, whereas excessive and constitutive activation of insulin/ IGF-1 signaling triggers NF-κB signaling and accelerates the aging process. It has been well documented that downregulation of insulin/IGF-1 can extend the life span in different species ranging from worms to mammals.…”

Section: P53 Insulin/igf-1 and Tor Pathwaysmentioning

confidence: 99%

The Regulation of Aging and Longevity: A New and Complex Role of p53

Feng

Lin

2011

Genes & Cancer

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Abstractp53 plays a critical role in tumor suppression. As a transcription factor, in response to stress signals, p53 regulates its target genes and initiates stress responses, including cell cycle arrest, apoptosis, and/or senescence, to exert its function in tumor suppression. Emerging evidence has suggested that p53 is also an important but complex player in the regulation of aging and longevity in worms, flies, mice, and humans. Whereas p53 accelerates the aging process and shortens life span in some contexts, p53 can also extend life span in some other contexts. Thus, p53 appears to regulate aging and longevity in a context-dependent manner. Here, the authors review some recent advances in the study of the role of p53 in the regulation of aging and longevity in both invertebrate and vertebrate models. Furthermore, they discuss the potential mechanisms by which p53 regulates aging and longevity, including the p53 regulation of insulin/TOR signaling, stem/progenitor cells, and reactive oxygen species.

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“…In mice, inactivation of SIRT6 leads to a premature aging phenotype and a dramatically shortened life span (Kriete and Mayo, 2009). SIRT6 binds to a subunit of NF-kappa B thereby restraining the activity of the transcription factor.…”

Section: Sirtuinsmentioning

confidence: 99%

How Environmental Agents Influence the Aging Process

Karol¹

2009

Biomolecules and Therapeutics

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-Aging is a multifaceted biological process that affects all organs and organ systems of the body. This review provides an up-to-date analysis of this highly exciting, rapidly changing field of science. The aging process is largely under genetic control but is highly responsive to diverse environmental influences. The genes that control aging are those that are involved with cell maintenance, cell damage and repair. The environmental factors that accelerate aging are those that influence either damage of cellular macromolecules, or interfere with their repair. Prominent among these are chronic inflammation, chronic infection, some metallic chemicals, ultraviolet light, and others that heighten oxidative stress. Other environment factors slow the aging process. Included among these agents are resveratrol and vitamin D. In addition, dietary restriction and exercise have been found to extend human lifespan. The various mechanisms whereby all these agents exert their influence on aging include epigenetic modification, chromatin maintenance, protection of telomeres, and anti-oxidant defense, among others. The complex process of aging remains under continued, intense investigation.

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Atypical pathways of NF-κB activation and aging

Cited by 77 publications

References 80 publications

Staphylococcus aureus regulates secretion of interleukin-6 and monocyte chemoattractant protein-1 through activation of nuclear factor kappaB signaling pathway in human osteoblasts

Staphylococcus aureus regulates secretion of interleukin-6 and monocyte chemoattractant protein-1 through activation of nuclear factor kappaB signaling pathway in human osteoblasts

The Regulation of Aging and Longevity: A New and Complex Role of p53

How Environmental Agents Influence the Aging Process

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