Tumor necrosis factors protect neurons against metabolic-excitotoxic insults and promote maintenance of calcium homeostasis

Cheng, Bin; Christakos, Sylvia; Mattson, Mark P.

doi:10.1016/0896-6273(94)90159-7

Cited by 631 publications

(383 citation statements)

References 103 publications

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“…IL-1a is believed to be one of the key factors in triggering brain immune responses by inducing the expressions of IL-6 , Frei et al, 1989 and TNFa (Bethea et al, 1992;Chung and Benveniste, 1990). In neuron, TNFa can modulate calcium channels (Soliven and Albert, 1992), decrease catecholamine secretion (Soliven and Albert, 1992), alter synaptic transmission (Tancredi et al, 1992) and protect CNS neurons against metabolic-excitotoxic insults and promote calcium homeostasis (Cheng et al, 1994). IL-6 can induce astrocyte to secrete nerve growth factor (Frei et al, 1989).…”

Section: Discussionmentioning

confidence: 99%

Expression of interleukin-1 alpha, tumor necrosis factor alpha and interleukin-6 genes in astrocytes under ischemic injury

Lau

2000

Neurochemistry International

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Section: Discussionmentioning

confidence: 99%

Expression of interleukin-1 alpha, tumor necrosis factor alpha and interleukin-6 genes in astrocytes under ischemic injury

Lau

2000

Neurochemistry International

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“…When pretreated with TNF, the neurons were more resistant to death when exposed to metabolic and excitotoxic insults. [57][58][59] Inhibiting NF-kB using a decoy DNA approach provided evidence that activation of NF-kB was necessary for the neuron survival-promoting action of TNF. 57 TNF pretreatment was associated with increased production of the antiapoptotic proteins Bcl-2 and Bcl-xL, and expression of a dominant negative form of IkB inhibited the ability of TNF to protect hippocampal neurons.…”

Section: Nf-jb As a Regulator Of Cell Survivalmentioning

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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“…Although it has been widely demonstrated that cerebral ischemia induces the expression of TNF-a in neurons, the effect of TNF-a on neuronal survival is unclear (Hallenbeck 2002). Accordingly, whereas some studies indicate that TNF-a has a deleterious effect in the acute phases of cerebral ischemia (Dawson et al, 1996;Barone et al, 1997), others have shown that induction of TNF-a is protective (Cheng et al, 1994;Nawashiro et al, 1997a;Ginis et al, 1999;Kirino 2002).…”

Section: Introductionmentioning

confidence: 99%

Tissue-Type Plasminogen Activator has a Neuroprotective Effect in the Ischemic Brain Mediated by Neuronal TNF-α

Haile

Echeverry

et al. 2011

J Cereb Blood Flow Metab

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Cerebral cortical neurons have a heightened sensitivity to hypoxia and their survival depends on their ability to accommodate to changes in the concentration of oxygen in their environment. Tissuetype plasminogen activator (tPA) is a serine proteinase that activates the zymogen plasminogen into plasmin. Hypoxia induces the release of tPA from cerebral cortical neurons, and it has been proposed that tPA mediates hypoxic and ischemic neuronal death. Here, we show that tPA is devoid of neurotoxic effects and instead is an endogenous neuroprotectant that renders neurons resistant to the effects of lethal hypoxia and ischemia. We present in vitro and in vivo evidence indicating that endogenous tPA and recombinant tPA induce the expression of neuronal tumor necrosis factor-a. This effect, mediated by plasmin and the N-methyl-D-aspartate receptor, leads to increased expression of the cyclin-dependent kinase inhibitor p21 and p21-mediated development of early hypoxic and ischemic tolerance.

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Tumor necrosis factors protect neurons against metabolic-excitotoxic insults and promote maintenance of calcium homeostasis

Cited by 631 publications

References 103 publications

Expression of interleukin-1 alpha, tumor necrosis factor alpha and interleukin-6 genes in astrocytes under ischemic injury

Expression of interleukin-1 alpha, tumor necrosis factor alpha and interleukin-6 genes in astrocytes under ischemic injury

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

Tissue-Type Plasminogen Activator has a Neuroprotective Effect in the Ischemic Brain Mediated by Neuronal TNF-α

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