TNF-α mediated transport of NF-κB to the nucleus is independent of the cytoskeleton-based transport system in non-neuronal cells

2006 ◽  
Vol 85 (6) ◽  
pp. 529-536 ◽  
Author(s):  
Ilja Mikenberg ◽  
Darius Widera ◽  
Aljoscha Kaus ◽  
Barbara Kaltschmidt ◽  
Christian Kaltschmidt
Keyword(s):  
Transport System ◽  
Neuronal Cells ◽  
Tnf Α

The Protective Effect of Picroside II on Isoflurane-Induced Neuronal Injury in Rats via Downregulating miR-195

2021 ◽  
pp. 1-9
Author(s):  
Hui Li ◽  
Weijia Du ◽  
Yawei Yuan ◽  
Jingjing Xue ◽  
Qiang Li ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Protective Effect ◽  
Inflammatory Cytokines ◽  
Escape Latency ◽  
Neuronal Cells ◽  
Neuronal Injury ◽  
Morris Water Maze Test ◽  
Picroside Ii ◽  
Tnf Α ◽  
Pro Inflammatory Cytokines

<b><i>Introduction:</i></b> Numerous pieces of evidence demonstrated that isoflurane induces hippocampal cell injury and cognitive impairments. Picroside II has been investigated for its anti-apoptosis and antioxidant neuroprotective effects. We aimed to explore the protective effects of picroside II and the role of microRNA-195 (miR-195) on isoflurane-induced neuronal injury in rats. <b><i>Methods:</i></b> The Morris water maze test was used to evaluate the effects of isoflurane on rats regarding escape latency and time in quadrant parameters. Real-time quantitative PCR was used to detect the expression levels of miR-195 and pro-inflammatory cytokines, including inter­leukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) mRNA, in the hippocampal tissues and neuronal cells. <b><i>Results:</i></b> The picroside II significantly improves isoflurane-induced higher escape latency and lower time spent in the quadrant compared with the control rats. Picroside II also promotes cell viability and suppresses cell apoptosis of isoflurane-induced neuronal cells. Besides, picroside II suppresses the expression of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) and miR-195 in vivo and in vitro. Furthermore, overexpression of miR-195 abrogates the effects of picroside II on the expression of pro-inflammatory cytokines. The appropriate dose of picroside II is 20 mg/kg. <b><i>Conclusion:</i></b> Picroside II could protect the nervous system possibly through inhibiting the inflammatory response in the isoflurane-induced neuronal injury of rats. The protective effect of picroside II may be achieved by downregulating the expression of miR-195 and then inhibiting the inflammatory response.

scholarly journals Proinflammatory cytokines induce accumulation of glypican-1-derived heparan sulfate and the C-terminal fragment of β-cleaved APP in autophagosomes of dividing neuronal cells

Glycobiology ◽  
2020 ◽  
Vol 30 (8) ◽  
pp. 539-549
Author(s):  
Fang Cheng ◽  
Lars-Åke Fransson ◽  
Katrin Mani
Keyword(s):  
Heparan Sulfate ◽  
Proinflammatory Cytokines ◽  
Polyacrylamide Gel Electrophoresis ◽  
Neuronal Cells ◽  
Sodium Dodecyl ◽  
Terminal Fragment ◽  
C Terminus ◽  
Tnf Α ◽  
Sds Page ◽  
N Terminus

Abstract Proinflammatory cytokines stimulate expression of β-secretase, which increases processing of amyloid precursor protein (APP), ultimately leading to the deposition of amyloid beta (Aβ). The N-terminal domain of β-cleaved APP supports Cu/NO-dependent release of heparan sulfate (HS) from the glypican-1 (Gpc-1) proteoglycan. HS is an inhibitor of β-secretase, thereby constituting a regulatory, negative feedback loop. Here, we have investigated the effect of the proinflammatory cytokines TNF-α, IL-1β and IL-6 on the interplay between APP processing and release of HS from Gpc-1 in neuronal cells. We have used deconvolution immunofluorescence microscopy and sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) and a panel of monoclonal/polyclonal antibodies recognizing the released HS, the N-terminus of Aβ, Aβ, the C-terminus of APP and the autophagosome marker LC3 as well as the chemical lysosome marker LysoTrackerRed (LTR). We repeatedly found that N2a neuroblastoma cells and human neural stem cells grown in the presence of the cytokines developed large cytoplasmic clusters, which stained positive for HS, the N-terminus of Aβ, Aβ, the C-terminus of APP, LC3 and LTR, indicating accumulation of HS and APP/APP degradation products in enlarged autophagosomes/lysosomes. The SDS-PAGE of immunoisolates obtained from TNF-α-treated N2a cells by using anti-C-terminus of APP revealed the presence of SDS-stable complexes between HS and the C-terminal fragment of β-cleaved APP (βCTF) migrating in the range 10–18 kDa. Clustered accumulation of βCTF disappeared when HS release was prevented and slightly enhanced when HS release was increased. Hence, when proinflammatory cytokines induce increased processing of APP, inhibition of β-secretase by HS is insufficient, which may lead to the impaired autophagosomal degradation.

Inhibition of PDE4 Attenuates TNF-α-Triggered Cell Death Through Suppressing NF-κB and JNK Activation in HT-22 Neuronal Cells

2019 ◽  
Vol 40 (3) ◽  
pp. 421-435 ◽  
Author(s):  
Jiao Xiao ◽  
Rumeng Yao ◽  
Bingtian Xu ◽  
Huizhen Wen ◽  
Jiahong Zhong ◽  
...  
Keyword(s):  
Cell Death ◽  
Neuronal Cells ◽  
Tnf Α ◽  
Jnk Activation

Reactive oxygen species‐dependent TNF‐α converting enzyme activation through stimulation of 5‐HT 2B and α 1D autoreceptors in neuronal cells

2005 ◽  
Vol 19 (9) ◽  
pp. 1078-1087 ◽  
Author(s):  
Mathéa Pietri ◽  
Benoît Schneider ◽  
Sophie Mouillet‐Richard ◽  
Myriam Ermonval ◽  
Vincent Mutel ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Neuronal Cells ◽  
Reactive Oxygen ◽  
Enzyme Activation ◽  
Oxygen Species ◽  
Converting Enzyme ◽  
Tnf Α ◽  
Stimulation Of

scholarly journals Betalain exerts a protective effect against glaucoma is majorly through the association of inflammatory cytokines

2020 ◽  
Author(s):  
Jiadi Wang ◽  
Dandan Zhang ◽  
Conghong Cao ◽  
Jing Yao
Keyword(s):  
Inflammatory Cytokines ◽  
Neuronal Cells ◽  
Protective Role ◽  
Marker Genes ◽  
Caveolin 1 ◽  
Tnf Α ◽  
Increased Activity ◽  
Cox 1

Abstract The present research aimed at evaluating the protective role of betalain on the in vitro glaucoma model using PC12 neuronal cells. The cultured neuronal cells in a customized pressurized chamber were analyzed for the onset of glutathione, myeloperoxidase (MPO), cathepsin, expression of inflammatory enzymes such as cyclooxygenase (COX-1), lipooxygenase (5- LOX), sPLA2 caveolin-1, glaucoma markers and other inflammatory cytokines in the presence and absence of betalain. The results have shown that a significant increase in the expression of oxidative stress with increased activity of cathepsin B and D. On the other hand, the activity of inflammatory enzymes such as COX-1, 5- LOX, sPLA2 were significantly increased in pressure exposed cells. In addition, glaucoma simulated cells demonstrated a significant increase in the VEGF, TGF-β, BDGF, and neuroserpin compared to control. Moreover, cells predisposed to hydrostatic pressure demonstrated an increase in (p<0.01) inflammatory cytokines such as IL-6, CXCR4, IL-17, IL-1β, and TNF-α levels. However, cells pre-treated with betalain improved the glutathione levels with attenuated MPO activity. Simultaneously, the levels of inflammatory cytokines and other glaucoma marker genes found restored in drug pre-treated cells. Thus, the results of the present study demonstrate that the use of betalain on ocular cells can prevent the progression of the disease that can be a suggestive therapeutic for controlling glaucoma like conditions.

scholarly journals Cellular prion protein coupling to TACE-dependent TNF-α shedding controls neurotransmitter catabolism in neuronal cells

2009 ◽  
Vol 110 (3) ◽  
pp. 912-923 ◽  
Author(s):  
Elodie Pradines ◽  
Damien Loubet ◽  
Sophie Mouillet-Richard ◽  
Philippe Manivet ◽  
Jean-Marie Launay ◽  
...  
Keyword(s):  
Prion Protein ◽  
Neuronal Cells ◽  
Cellular Prion Protein ◽  
Protein Coupling ◽  
Tnf Α

scholarly journals Astrocytic adenosine: from synapses to psychiatric disorders

2014 ◽  
Vol 369 (1654) ◽  
pp. 20130594 ◽  
Author(s):  
Dustin J. Hines ◽  
Philip G. Haydon
Keyword(s):  
Psychiatric Disorders ◽  
Neuronal Cells ◽  
Atp Release ◽  
General Term ◽  
The Body ◽  
Signalling Molecules ◽  
Major Class ◽  
Tnf Α ◽  
The Brain ◽  
Complex Organ

Although it is considered to be the most complex organ in the body, the brain can be broadly classified into two major types of cells, neuronal cells and glial cells. Glia is a general term that encompasses multiple types of non-neuronal cells that function to maintain homeostasis, form myelin, and provide support and protection for neurons. Astrocytes, a major class of glial cell, have historically been viewed as passive support cells, but recently it has been discovered that astrocytes participate in signalling activities both with the vasculature and with neurons at the synapse. These cells have been shown to release d -serine, TNF-α, glutamate, atrial natriuretic peptide (ANP) and ATP among other signalling molecules. ATP and its metabolites are well established as important signalling molecules, and astrocytes represent a major source of ATP release in the nervous system. Novel molecular and genetic tools have recently shown that astrocytic release of ATP and other signalling molecules has a major impact on synaptic transmission. Via actions at the synapse, astrocytes have now been shown to regulate complex network signalling in the whole organism with impacts on respiration and the sleep–wake cycle. In addition, new roles for astrocytes are being uncovered in psychiatric disorders, and astrocyte signalling mechanisms represents an attractive target for novel therapeutic agents.

Selected Contribution: Circadian rhythm of tumor necrosis factor-α uptake into mouse spinal cord

2002 ◽  
Vol 92 (3) ◽  
pp. 1357-1362 ◽  
Author(s):  
Weihong Pan ◽  
Germaine Cornélissen ◽  
Franz Halberg ◽  
Abba J. Kastin
Keyword(s):  
Spinal Cord ◽  
Circadian Rhythm ◽  
Tumor Necrosis Factor ◽  
Transport System ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Circadian Variation ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Circadian variations in the actions of tumor necrosis factor-α (TNF-α) have been observed. Because a saturable transport system at the blood-brain barrier mediates most of the influx of TNF-α from blood to the central nervous system (CNS), the circadian variation of the CNS effects of TNF-α could be related to changes in this transport system. Accordingly, we measured the uptake of intravenously injected TNF-α into various CNS regions at different times and compared these measurements with the uptake into a peripheral control (muscle). We found that the spinal cord, but not the brain, showed a circadian rhythm in the uptake of TNF-α. This pattern is similar to that of leptin but different from that of interleukin-1. The circadian rhythm of the influx of TNF-α into this region of the CNS suggests a functional role for the spinal cord in the physiological actions of TNF-α.

scholarly journals Betalain exerts protective effect against glaucoma is majorly through the association of inflammatory cytokines

2020 ◽  
Author(s):  
Jiadi Wang ◽  
Dandan Zhang ◽  
Conghong Cao ◽  
Jing Yao
Keyword(s):  
Inflammatory Cytokines ◽  
Neuronal Cells ◽  
Protective Role ◽  
Marker Genes ◽  
Caveolin 1 ◽  
Tnf Α ◽  
Increased Activity ◽  
Cox 1

Abstract The present research aimed at evaluating the protective role of betalain on the in vitro glaucoma model using PC12 neuronal cells. The cultured neuronal cells in a customized pressurized chamber were analyzed for the onset of glutathione, myeloperoxidase (MPO), cathepsin, expression of inflammatory enzymes such as cyclooxygenase (COX-1), lipooxygenase (5- LOX), sPLA2 caveolin-1, glaucoma markers and other inflammatory cytokines in the presence and absence of betalain. The results shown that a significant increase in the expression of oxidative stress with increased activity of cathepsin B and D. On the other hand, the activity of inflammatory enzymes such as COX-1, 5- LOX, sPLA2 were significantly increased in pressure exposed cells. In addition, glaucoma simulated cells demonstrated cells displayed a significant increase in the VEGF, TGF-β, BDGF and neuroserpin compared to control. Moreover, cells predisposed to hydrostatic pressure demonstrated an increase in (p<0.01) inflammatory cytokines such as IL-6, CXCR4, IL-17, IL-1β, and TNF-α levels. However, cells pre-treated with betalain improved the glutathione levels with attenuated MPO activity. Simultaneously, the levels of inflammatory cytokines and other glaucoma marker genes were found to restore in drug pre-treated cells. Thus, the results of the present study demonstrate that the use of betalain on ocular cells can prevent the progression of the disease that can be a suggestive therapeutic for controlling glaucoma like conditions.

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