Signaling via NF-κB in the nervous system

Kaltschmidt, Barbara; Widera, Darius; Kaltschmidt, Christian

doi:10.1016/j.bbamcr.2005.05.009

Cited by 267 publications

(229 citation statements)

References 168 publications

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“…Furthermore, we observed the activation of Akt and NF-κB (p65) (Fig. 2h), and a significant upregulation of their downstream transcriptional targets, Bcl-2 and Bcl-xL 20,23 (Fig. 2i), at 7 DAT in the NSPC-transplanted group, resulting in decreased activation of caspases 9 and 3 ( Fig.…”

Section: Cell Viability and Functional Improvementmentioning

confidence: 93%

“…Because these neurohumoral factors prevent neural apoptosis by the activation of the PI3K-Akt/NF-κB signalling pathway in vitro [20][21][22][23] , the neuroprotective effects through NSPC transplantation were examined. Histopathological examinations at 7 DAT revealed fewer TUNEL-positive cells and more spared myelin in the NSPC-transplanted group (Fig.…”

Section: Cell Viability and Functional Improvementmentioning

confidence: 99%

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Direct isolation and RNA-seq reveal environment-dependent properties of engrafted neural stem/progenitor cells

et al. 2012

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neural stem/progenitor cell (nsPC) transplantation is a promising treatment for various neurodegenerative disorders including spinal cord injury, however, no direct analysis has ever been performed on their in vivo profile after transplantation. Here we combined bioimaging, flow-cytometric isolation and ultra-high-throughput RnA sequencing to evaluate the cellular properties of engrafted nsPCs. The acutely transplanted nsPCs had beneficial effects on spinal cord injury, particularly neuroprotection and neurohumoral secretion, whereas their in situ secretory activity differed significantly from that predicted in vitro. The RnA-sequencing of engrafted nsPCs revealed dynamic expression/splicing changes in various genes involved in cellular functions and tumour development depending on graft environments. notably, in the pathological environment, overall transcriptional activity, external signal transduction and neural differentiation of engrafted nsPCs were significantly suppressed. These results highlight the vulnerability of engrafted nsPCs to environmental force, while emphasizing the importance of in situ analysis in advancing the efficacy and safety of stem cell-based therapies.

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Section: Cell Viability and Functional Improvementmentioning

confidence: 93%

Section: Cell Viability and Functional Improvementmentioning

confidence: 99%

Direct isolation and RNA-seq reveal environment-dependent properties of engrafted neural stem/progenitor cells

et al. 2012

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“…As the latter and other findings have been the subject of several recent reviews, we will not detail them here. 25,26 Whether different subunits of the NF-kB family will have primarily overlapping, or some distinct, Figure 1 Protein modifications and interactions involved in the activation of NF-kB and the regulation of gene expression by this transcription factor. In the canonical pathway of NF-kB activation, incoming signals activate the IkB kinases (IKKa and IKKb), which then phosphorylate IkBa.…”

Section: Plasticity and Growth Cognitive Functionmentioning

confidence: 99%

“…Several studies have revealed new transcriptional targets of NF-kB in the brain, as described in a current review. 26 Interestingly, a general role for NF-kB-mediated transcriptional regulation in long-term memory was recently revealed in a microarray study. Levenson, Sweatt, and co-workers conducted a bioinformatics analysis of transcripts with altered expression levels during NMDA-receptor-dependent contextual memory consolidation.…”

Section: Plasticity and Growth Cognitive Functionmentioning

confidence: 99%

Roles for NF-κB in nerve cell survival, plasticity, and disease

2006

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Here we review evidence of roles for NF-jB in the regulation of developmental and synaptic plasticity, and cell survival in physiological and pathological settings. Signaling pathways modulating NF-jB activity include those engaged by neurotrophic factors, neurotransmitters, electrical activity, cytokines, and oxidative stress. Emerging findings support a pivotal role for NF-jB as a mediator of transcription-dependent enduring changes in the structure and function of neuronal circuits. Distinct subunits of NF-jB may uniquely affect cognition and behavior by regulating specific target genes. NF-jB activation can prevent the death of neurons by inducing the production of antiapoptotic proteins such as Bcl-2, IAPs and manganese superoxide dismutase (Mn-SOD). Recent findings indicate that NF-jB plays important roles in disorders such as epilepsy, stroke, Alzheimer's and Parkinson's diseases, as well as oncogenesis. Molecular pathways upstream and downstream of NF-jB in neurons are being elucidated and may provide novel targets for therapeutic intervention in various neurological disorders.

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“…Activated NF-kB subsequently alters the transcription of a large number of genes, most of which participate in innate immunity, inflammation, and cell survival [1,2]. NF-kB is highly activated at sites of inflammation in a wide range of human diseases including cancer [3], rheumatic diseases [4], inflammatory bowel diseases [5], neurodegenerative conditions [6], asthma and chronic obstructive pulmonary disease [7].…”

Section: Introductionmentioning

confidence: 99%

Molecular imaging of NF‐kappaB in prostate tissue after systemic administration of IL‐1β

et al. 2007

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BACKGROUND. Activation of nuclear-factor kappaB (NF-kB) influences the transcription of number of genes, many of which participate in inflammatory responses and tumor development. A wide range of human cancers and inflammatory disorders express inappropriate regulation of NF-kB. The role of NF-kB in intraprostatic inflammation has not been elucidated. METHODS. Using transgenic NF-kB-Luciferase Tag mice coupled to the luciferase reporter gene, we performed serial, noninvasive in vivo and ex vivo molecular imaging of NF-kB activation in the mouse body after systemic administration of mouse pro-inflammatory cytokines: TNF-a, IL-6, and IL-1b at 10 mg/kg body weights. In some experiments, pretreatment with dexamethasone (10 mg/kg) was used to modulate the cytokine-induced NF-kB-dependent luminescence in vivo. RESULTS. Treatment of NF-kB-Luc mice with cytokines increased luminescence in a time-and organ-specific manner. Highest levels of NF-kB-dependent luminescence were observed approximately 3-4 hr after IL-1b administration. An important finding was the cumulative effect of IL-1b to activate NF-kB in the prostate during chronic administration. CONCLUSIONS. The molecular imaging of NF-kB activity might be an attractive approach to distinguish the role of cytokine-induced NF-kB signaling in intraprostatic inflammation and prostate cancer development. Since dexamethasone, a known NF-kB inhibitor, could reduce the IL-1b-induced NF-kB-dependent luminescence in the prostate, NF-kB-Luc mice might be useful tool to screen potential candidate drugs for treatment of inflammation and tumor associated with aberrant NF-kB activity.

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Signaling via NF-κB in the nervous system

Cited by 267 publications

References 168 publications

Direct isolation and RNA-seq reveal environment-dependent properties of engrafted neural stem/progenitor cells

Direct isolation and RNA-seq reveal environment-dependent properties of engrafted neural stem/progenitor cells

Roles for NF-κB in nerve cell survival, plasticity, and disease

Molecular imaging of NF‐kappaB in prostate tissue after systemic administration of IL‐1β

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