NF-κB 在中枢神经系统损伤和修复中的作用

Yang, Li; Tao, Luyang; Chen, Xiping

doi:10.1007/s12264-007-0046-6

Cited by 49 publications

(31 citation statements)

References 33 publications

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“…Although NF-B has been linked to both neurodegeneration and neuroprotection [76] , most studies have concentrated on the role of NF-B in the pathogenesis of neuropathic pain [77][78][79][80][81] . Nevertheless, studies of inflammatory demyelination in the peripheral nervous system have shown that NF-B and its inhibitor, I-B, are expressed in macrophages and SCs, possibly regulating the demyelination process [82,83] .…”

Section: Proinflammatory Transcription Factorsmentioning

confidence: 99%

Molecular Inflammatory Mediators in Peripheral Nerve Degeneration and Regeneration

Cámara-Lemarroy

Garza²,

Fernández-Garza³

2010

Neuroimmunomodulation

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Wallerian degeneration, the self-destructive set of cellular and molecular processes by which degenerating axons and myelin are cleared after injury, is initiated by macrophages and Schwann cells. Molecular inflammatory mediators such as cytokines (IL-1, IL-6, IL-10, and TNF-α, among others), transcription factors (NF-ĸB, c-Jun), the complement system and arachidonic acid metabolites have been shown to modulate these processes in various studies. However, the exact role that each of these mediators plays during axonal degeneration and regeneration has not been fully established. Understanding the molecular basis of these interactions between the immune system and peripheral nerve injury would open the possibility of targeting these inflammatory mediators as therapeutic interventions. In this review we attempt to integrate the current evidence generated around this issue, and to explore the therapeutic possibilities that arise.

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Section: Proinflammatory Transcription Factorsmentioning

confidence: 99%

Molecular Inflammatory Mediators in Peripheral Nerve Degeneration and Regeneration

Cámara-Lemarroy

Garza²,

Fernández-Garza³

2010

Neuroimmunomodulation

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“…The role of NF-κB in apoptosis remains controversial. NF-κB has been demonstrated to promote cell proliferation and protect the cell from apoptosis [19] . The anti-apoptosis function of NF-κB most likely occurs through suppression of tumor necrosis factor α (TNF-α) signaling [20] .…”

Section: Activation Of Nf-κb-and Caspase-3-dependent Apoptosismentioning

confidence: 99%

Expression of the apoptosis-related proteins caspase-3 and NF-κB in the hippocampus of Tg2576 mice

Niu

Zhang

et al. 2010

Neurosci. Bull.

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Objective To investigate the relations between neuroapoptosis and the onset and development of Alzheimer's disease (AD), especially the role of NF-κB in the regulation of neuroapoptosis. Methods expressions in the CA3 region of the hippocampus in APPswe Tg2576 transgenic mice were studied from postnatal day 0-180, using Nissl staining, immunohistochemistry and RT-PCR methods. Results Both neuronal apoptosis and NF-κB activity decreased gradually with the increase of age in wild type and Tg2576 mice. However, the number of caspase-3-positive or NF-κB-positive pyramidal cells in Tg2576 mice was greater than that in age-matched wild type mice, with significant differences after postnatal day 14 (P < 0.01 or P < 0.05). Linear regression analyses of caspase-3 and NF-κB expression demonstrated a correlation between neuroapoptosis and activity of NF-κB. Conclusion The process of neuroapoptosis is consistent with the onset and development of AD. Furthermore, the observed correlation between neuroapoptosis and NF-κB activity suggests a role of NF-κB in hippocampal neuroapoptosis.

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“…Inflammatory stimuli activate the IB kinase (IKK) complex, which phosphorylates IB, leading to its ubiquitination and subsequent degradation. IB degradation facilitates translocation of NF-B to the nucleus, thereby regulating the transcription of genes involved in human disorders, including cancer, neurodegenerative disease, and obesity-related metabolic disease (11)(12)(13). NF-B is also involved in cancer-induced cachexia, because intratumoral injection of NF-B inhibitory oligonucleotides prevents cachexia in a mouse tumor model (14).…”

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confidence: 99%

NF-κB Activation in Hypothalamic Pro-opiomelanocortin Neurons Is Essential in Illness- and Leptin-induced Anorexia

Jang

Namkoong

Kang

et al. 2010

Journal of Biological Chemistry

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Anorexia and weight loss are prevalent in infectious diseases. To investigate the molecular mechanisms underlying these phenomena, we established animal models of infection-associated anorexia by administrating bacterial and viral products, lipopolysaccharide (LPS) and human immunodeficiency virus-1 transactivator protein (Tat). In these models, we found that the nuclear factor-B (NF-B), a pivotal transcription factor for inflammation-related proteins, was activated in the hypothalamus. In parallel, administration of LPS and Tat increased hypothalamic pro-inflammatory cytokine production, which was abrogated by inhibition of hypothalamic NF-B. In vitro, NF-B activation directly stimulated the transcriptional activity of proopiomelanocortin (POMC), a precursor of anorexigenic melanocortin, and mediated the stimulatory effects of LPS, Tat, and pro-inflammatory cytokines on POMC transcription, implying the involvement of NF-B in controlling feeding behavior. Consistently, hypothalamic injection of LPS and Tat caused a significant reduction in food intake and body weight, which was prevented by blockade of NF-B and melanocortin. Furthermore, disruption of IB kinase-␤, an upstream kinase of NF-B, in POMC neurons attenuated LPS-and Tat-induced anorexia. These findings suggest that infection-associated anorexia and weight loss are mediated via NF-B activation in hypothalamic POMC neurons. In addition, hypothalamic NF-B was activated by leptin, an important anorexigenic hormone, and mediates leptin-stimulated POMC transcription, indicating that hypothalamic NF-B also serves as a downstream signaling pathway of leptin.

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NF-κB 在中枢神经系统损伤和修复中的作用

Cited by 49 publications

References 33 publications

Molecular Inflammatory Mediators in Peripheral Nerve Degeneration and Regeneration

Molecular Inflammatory Mediators in Peripheral Nerve Degeneration and Regeneration

Expression of the apoptosis-related proteins caspase-3 and NF-κB in the hippocampus of Tg2576 mice

NF-κB Activation in Hypothalamic Pro-opiomelanocortin Neurons Is Essential in Illness- and Leptin-induced Anorexia

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