Trail interacts redundantly with nitric oxide in rat astrocytes: Potential contribution to neurodegenerative processes

Cantarella, Giuseppina; Lempereur, Laurence; D'Alcamo, Maria; Risuglia, Nunziata; Cardile, Venera; Pennisi, G; Scoto, G.M.; Bernardini, Renato

doi:10.1016/j.jneuroim.2006.09.007

Cited by 25 publications

(19 citation statements)

References 31 publications

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“…TRAIL can preferentially induce apoptosis via five active transmembrane death receptors, which include DR4 and DR5 in a variety of tumor cell types (Sage et al, 2014), whereas normal cells do not appear to be sensitive (Zhuang et al, 2013). In our case TRAIL expression showed no differences among groups despite data from literature supporting TRAIL-NO interactions (Cantarella et al, 2007). RCA and HT-CA contact could involve in particular TRAIL receptors.…”

Section: Discussioncontrasting

confidence: 49%

Raw and thermally treated cement asbestos exerts different cytotoxicity effects on A549 cells in vitro

et al. 2015

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Section: Discussioncontrasting

confidence: 49%

Raw and thermally treated cement asbestos exerts different cytotoxicity effects on A549 cells in vitro

et al. 2015

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“…To confirm the specificity of detrimental effects of TRAIL in SCI, we found that the expression of the cell death-related phosphorylated form of kinase JNK was increased 24 h after SCI in spinal cords. Increased phosphorylation of JNK has been reported after treatment with TRAIL in other in vivo and also in in vitro models (Corazza et al, 2006;Jurewicz et al, 2006;Cantarella et al, 2007) and represents a step of the canonical transduction pathway set into motion after binding of TRAIL to its DR5 death receptor (Jaganathan et al, 2002). Thus, it seemed obvious that prevention of TRAIL detrimental effects in SCI by means of TRAILneutralizing antibody was associated with decrease activation of the death-related kinase JNK.…”

Section: Discussionmentioning

confidence: 98%

Neutralization of Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand Reduces Spinal Cord Injury Damage in Mice

Cantarella

Benedetto

Scollo

et al. 2010

Neuropsychopharmacol

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Spinal cord injury (SCI) is a major cause of disability, its clinical outcome depending mostly on the extent of damage in which proapoptotic cytokines have a crucial function. In particular, the inducers of apoptosis belonging to TNF receptor superfamily and their respective ligands are upregulated after SCI. In this study, the function of the proapoptotic cytokine tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in SCI-induced damage was investigated in the mouse. SCI resulted in severe trauma, characterized by prominent inflammation-related damage and apoptosis. Immunostaining for TRAIL and its receptor DR5 was found in the white and gray matter of the perilesional area, as also confirmed by western blotting experiments. Immunoneutralization of TRAIL resulted in improved functional recovery, reduced apoptotic cell number, modulation of molecules involved in the inflammatory response (FasL, TNF-a, IL-1b, and MPO), and the corresponding signaling (caspase-8 and -3 activation, JNK phosphorylation, Bax, and Bcl-2 expression). As glucocorticoid-induced TNF receptor superfamily-related protein (GITR) activated by its ligand (GITRL) contributes to SCI-related inflammation, interactions between TRAIL and GITRL were investigated. SCI was associated with upregulated GITR and GITRL expression, a phenomenon prevented by anti-TRAIL treatment. Moreover, the expression of both TRAIL and DR5 was reduced in tissues from mice lacking the GITR gene (GITR À/À ) in comparison with wild-type mice suggesting that TRAIL-and GITRL-activated pathways synergise in the development of SCI-related inflammatory damage. Characterization of new targets within such molecular systems may constitute a platform for innovative treatment of SCI.

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“…11, 21, 22, 23 As such, TRAIL signaling also promotes an array of biological responses associated with cellular growth and survival. 24 In line with these findings, we report novel evidence here that TRAIL is upregulated in the ischemic brains of animals subjected to focal ischemia, whereas it appears dramatically downregulated in the brains of animals subjected to a sub-lethal ischemia, PC, or an harmful ischemia preceded by PC.…”

Section: Discussionmentioning

confidence: 99%

“…TNF-related apoptosis inducing ligand (TRAIL), a proapoptotic member of the TNF superfamily released by glia 10, 11 and injured neurons, 12 appears to trigger apoptosis following focal brain ischemia. 13 TRAIL binds five receptors, death receptor-4 (DR4), DR5, decoy receptor 1 (DcR1), DcR2, and osteoprogeterin.…”

mentioning

confidence: 99%

Ischemic tolerance modulates TRAIL expression and its receptors and generates a neuroprotected phenotype

Cantarella

Pignataro²,

Benedetto

et al. 2014

Cell Death Dis

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TNF-related apoptosis inducing ligand (TRAIL), a member of the TNF superfamily released by microglia, appears to be involved in the induction of apoptosis following focal brain ischemia. Indeed, brain ischemia is associated with progressive enlargement of damaged areas and prominent inflammation. As ischemic preconditioning reduces inflammatory response to brain ischemia and ameliorates brain damage, the purpose of the present study was to evaluate the role of TRAIL and its receptors in stroke and ischemic preconditioning and to propose, by modulating TRAIL pathway, a new therapeutic strategy in stroke. In order to achieve this aim a rat model of harmful focal ischemia, obtained by subjecting animals to 100 min of transient occlusion of middle cerebral artery followed by 24 h of reperfusion and a rat model of ischemic preconditioning in which the harmful ischemia was preceded by 30 mins of tMCAO, which represents the preconditioning protective stimulus, were used. Results show that the neuroprotection elicited by ischemic preconditioning occurs through both upregulation of TRAIL decoy receptors and downregulation of TRAIL itself and of its death receptors. As a counterproof, immunoneutralization of TRAIL in tMCAO animals resulted in significant restraint of tissue damage and in a marked functional recovery. Our data shed new light on the mechanisms that propagate ongoing neuronal damage after ischemia in the adult mammalian brain and provide new molecular targets for therapeutic intervention. Strategies aimed to repress the death-inducing ligands TRAIL, to antagonize the death receptors, or to activate the decoy receptors open new perspectives for the treatment of stroke.

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Trail interacts redundantly with nitric oxide in rat astrocytes: Potential contribution to neurodegenerative processes

Cited by 25 publications

References 31 publications

Raw and thermally treated cement asbestos exerts different cytotoxicity effects on A549 cells in vitro

Raw and thermally treated cement asbestos exerts different cytotoxicity effects on A549 cells in vitro

Neutralization of Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand Reduces Spinal Cord Injury Damage in Mice

Ischemic tolerance modulates TRAIL expression and its receptors and generates a neuroprotected phenotype

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