Formation of a tumour necrosis factor receptor 1 molecular scaffolding complex and activation of apoptosis signal‐regulating kinase 1 during seizure‐induced neuronal death

Shinoda, Sachiko; Skradski, Shana L.; Araki, Toshimitsu; Schindler, Clara K.; Meller, Robert; Lan, Jing-Quan; Taki, Waro; Simon, Roger P.; Henshall, David C.

doi:10.1046/j.1460-9568.2003.02655.x

Cited by 89 publications

(94 citation statements)

References 67 publications

(123 reference statements)

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“…The data presented here confirm and extend these observations and demonstrate that after TBI, cIAP-1 dissociates and cIAP-2 increases association with TNFR1 in the cholesterolsphingolipid-enriched membrane microdomains. In support of this observation, the TNFR1 signaling complex during seizureinduced neuronal death contains cIAP-2 (Shinoda et al, 2003). Thus, the amount of cIAP-1 or cIAP-2 recruited to the engaged TNFR1 is critical for the net function of the signaling complex; however, our data do not reveal whether the extensive modifications of adaptor proteins seen after TBI mediate associations of cIAPs with the receptor complex.…”

Section: Discussionsupporting

confidence: 46%

“…Tumor necrosis factor (TNF)-␣ is a prominent proinflammatory cytokine that has been associated with various neurodegenerative diseases (Tyor et al, 1995;Clark and Lutsep, 2001;Lou et al, 2001;Perry et al, 2001;Probert and Akassoglou, 2001;Shinoda et al, 2003). Its function in the pathogenesis of neural injury remains unclear, however, because both neurotoxic and neuroprotective effects after injury have been described (Bruce et al, 1996;Nawashiro et al, 1997;Kim et al, 2001;Martin-Villalba et al, 2001;Yang et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

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Tumor Necrosis Factor Receptor 1 and Its Signaling Intermediates Are Recruited to Lipid Rafts in the Traumatized Brain

Lotocki¹,

Alonso

Dietrich³

et al. 2004

J. Neurosci.

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The tumor necrosis factor (TNF) ligand-receptor system plays an essential role in apoptosis that contributes to secondary damage after traumatic brain injury (TBI). TNF also stimulates inflammation by activation of gene transcription through the IB kinase (IKK)/NF-B and JNK (c-Jun N-terminal protein kinase)/AP-1 signaling cascades. The mechanism by which TNF signals between cell death and survival and the role of receptor localization in the activation of downstream signaling events are not fully understood. Here, TNF receptor 1 (TNFR1) signaling complexes in lipid rafts were investigated in the cerebral cortex of adult male Sprague Dawley rats subjected to moderate (1.8 -2.2 atmospheres) fluid-percussion TBI and naive controls. In the normal rat cortex, a portion of TNFR1 was present in lipid raft microdomains, where it associated with the adaptor proteins TRADD (TNF receptor-associated death domain), TNF receptorassociated factor-2 (TRAF-2), the Ser/Thr kinase RIP (receptor-interacting protein), TRAF1, and cIAP-1 (cellular inhibitor of apoptosis protein-1), forming a survival signaling complex. Moderate TBI resulted in rapid recruitment of TNFR1, but not TNFR2 or Fas, to lipid rafts and induced alterations in the composition of signaling intermediates. TNFR1 and TRAF1 were polyubiquitinated in lipid rafts after TBI. Subsequently, the signaling complex contained activated caspase-8, thus initiating apoptosis. In addition, TBI caused a transient activation of NF-B, but receptor signaling interacting proteins IKK␣ and IKK␤ were not detected in raft-containing fractions. Thus, redistribution of TNFR1 in lipid rafts and nonraft regions of the plasma membrane may regulate the diversity of signaling responses initiated by these receptors in the normal brain and after TBI.

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Section: Discussionsupporting

confidence: 46%

Section: Introductionmentioning

confidence: 99%

Tumor Necrosis Factor Receptor 1 and Its Signaling Intermediates Are Recruited to Lipid Rafts in the Traumatized Brain

Lotocki¹,

Alonso

Dietrich³

et al. 2004

J. Neurosci.

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“…35) Seizure-induced mitochondrial dysfunction and activation of Bcl-2 family are calcium dependent or at least partly of calcium dependent, 38,39) whereas a role for death receptors contributing to seizure-induced neuronal death is less likely because there is no apparent requirement for calcium in the activation mechanism. 35,40) Our results suggest that the neuroprotective effect of PIP should be calcium dependent and participate in protecting intracellular organelles, such as mitochondrion and endoplasmic reticulum (ER).…”

Section: Discussionmentioning

confidence: 90%

Neuroprotective Effect of Piperine on Primarily Cultured Hippocampal Neurons

Sun

Zuo

2010

Biological & Pharmaceutical Bulletin

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It was previously reported that piperine (PIP) significantly blocks convulsions induced by intracerebroventricular injection of threshold doses of kainate, but had no or only slight effects on convulsions induced by L-glutamate, N-methyl-D-aspartate and guanidinosuccinate. In traditional Chinese medicine, black pepper has been used for epileptic treatment; however, the exact mechanism is still unclear. We reported here in that appropriate concentration of PIP effectively inhibites the synchronized oscillation of intracellular calcium in rat hippocampal neuronal networks and represses spontaneous synaptic activities in terms of spontaneous synaptic currents (SSC) and spontaneous excitatory postsynaptic currents (sEPSC). Moreover, pretreatment with PIP expects protective effect on glutamate-induced decrease of cell viability and apoptosis of hippocampal neurons. These data suggest that the neuroprotective effects of PIP might be associated with suppression of synchronization of neuronal networks, presynaptic glutamic acid release, and Ca 2؉ overloading.

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“…Brain TNFα production is increased during seizures and contributes to neuronal death [122,125,126]. TNFα also directly targets the cerebral vasculature [44].…”

Section: Seizures Neuronal Injury and Cerebral Vascular Functionmentioning

confidence: 99%

Cerebroprotective Functions of HO-2

Parfenova¹,

Leffler²

2008

CPD

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The constitutive isoform of heme oxygenase, HO-2, is highly expressed in the brain and in cerebral vessels. HO-2 functions in the brain have been evaluated using pharmacological inhibitors of the enzyme and HO-2 gene deletion in in vivo animal models and in cultured cells (neurons, astrocytes, cerebral vascular endothelial cells). Rapid activation of HO-2 via posttranslational modifications without upregulation of HO-2 expression or HO-1 induction coincides with the increase in cerebral blood flow aimed at maintaining brain homeostasis and neuronal survival during seizures, hypoxia, and hypotension. Pharmacological inhibition or gene deletion of brain HO-2 exacerbates oxidative stress induced by seizures, glutamate, and inflammatory cytokines, and causes cerebral vascular injury. Carbon monoxide (CO) and bilirubin, the end products of HO-catalyzed heme degradation, have distinct cytoprotective functions. CO, by binding to a heme prosthetic group, regulates the key components of cell signaling, including BK Ca channels, guanylyl cyclase, NADPH oxidase, and the mitochondria respiratory chain. Cerebral vasodilator effects of CO are mediated via activation of BK Ca channels and guanylyl cyclase. CO, by inhibiting the major components of endogenous oxidantgenerating machinery, NADPH oxidase and the cytochrome C oxidase of the mitochondrial respiratory chain, blocks formation of reactive oxygen species. Bilirubin, via redox cycling with biliverdin, is a potent oxidant scavenger that removes preformed oxidants. Overall, HO-2 has dual housekeeping cerebroprotective functions by maintaining autoregulation of cerebral blood flow aimed at improving neuronal survival in a changing environment, and by providing an effective defense mechanism that blocks oxidant formation and prevents cell death caused by oxidative stress. KeywordsHeme oxygenase; cerebral protection; cerebrovascular disease; oxidative stress; seizures; carbon monoxide; bilirubin Vasodilator role of CO in cerebral circulation A. Vasoactive effects of exogenous CO in cerebral vesselsExperimental studies in newborn pigs conducted using in vivo and in vitro approaches demonstrate that exogenous CO is a potent vasodilator in cerebral circulation [1][2][3][4][5][6][7]. CO can be delivered to the brain as CO gas dissolved in a physiological buffer or as recently introduced CO-releasing molecules (CO-RMs) that release CO on illumination (dimanganese decacarbonyl, DMDC) or when dissolved in physiologically buffered solutions (sodium boranocarbonate, CO-RM-A1) [8,9]. In vivo, CO, DMDC and CORM-A1 applied directly to the brain surface under the cranial window at concentrations ≥10 −7 M causes dilation of pial arterioles, major resistance brain vessels that define the cerebral blood

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Formation of a tumour necrosis factor receptor 1 molecular scaffolding complex and activation of apoptosis signal‐regulating kinase 1 during seizure‐induced neuronal death

Cited by 89 publications

References 67 publications

Tumor Necrosis Factor Receptor 1 and Its Signaling Intermediates Are Recruited to Lipid Rafts in the Traumatized Brain

Tumor Necrosis Factor Receptor 1 and Its Signaling Intermediates Are Recruited to Lipid Rafts in the Traumatized Brain

Neuroprotective Effect of Piperine on Primarily Cultured Hippocampal Neurons

Cerebroprotective Functions of HO-2

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