ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2010
Neutralization of tumor necrosis factor-related apoptosis-inducing ligand reduces spinal cord injury damage in mice.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Caspase-8 expression in CD8Science advances · 2025Article
- Tibolone Improves Motor Recovery and Regulates Neuroinflammation and Gliosis in a Model of Traumatic Spinal Cord Injury.International journal of molecular sciences · 2025Article
- Association of circulating cytokine levels and tissue-infiltrating myeloid cells with achalasia: results from Mendelian randomization and validation through clinical characteristics and single-cell RNA sequencing.Journal of gastroenterology · 2024Article
- Indirubin Inhibits TRAIL-Induced Activation of Death Receptor 5 in Jurkat Cells.Natural product communications · 2023Article
- TRAIL-R Deficient Mice Are Protected from Neurotoxic Effects of Amyloid-β.International journal of molecular sciences · 2022Article
- Elucidating the Potential Mechanisms Underlying Distraction Spinal Cord Injury-Associated Neuroinflammation and Apoptosis.Frontiers in cell and developmental biology · 2022Article
- Inflammation after spinal cord injury: a review of the critical timeline of signaling cues and cellular infiltration.Journal of neuroinflammation · 2021Review
- Targeting the miRNA-155/TNFSF10 network restrains inflammatory response in the retina in a mouse model of Alzheimer's disease.Cell death & disease · 2021Article
- The immune system on the TRAIL of Alzheimer's disease.Journal of neuroinflammation · 2020Review
- Insight into the divergent role of TRAIL in non-neoplastic neurological diseases.Journal of cellular and molecular medicine · 2020Review
- Beneficial effects of curtailing immune susceptibility in an Alzheimer's disease model.Journal of neuroinflammation · 2019Article
- Regulation of Inflammatory Cytokines for Spinal Cord Injury Repair Through Local Delivery of Therapeutic Agents.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2018Review
- Role of Caspase-8 and Fas in Cell Death After Spinal Cord Injury.Frontiers in molecular neuroscience · 2018Review
- Retrograde Activation of the Extrinsic Apoptotic Pathway in Spinal-Projecting Neurons after a Complete Spinal Cord Injury in Lampreys.BioMed research international · 2017Article
- Neutralization of TNFSF10 ameliorates functional outcome in a murine model of Alzheimer's disease.Brain : a journal of neurology · 2015Article
- Complex changes in the apoptotic and cell differentiation programs during initiation of the hair follicle response to chemotherapy.The Journal of investigative dermatology · 2014Article
- Ischemic tolerance modulates TRAIL expression and its receptors and generates a neuroprotected phenotype.Cell death & disease · 2014Article
- Blockade of Death Ligand TRAIL Inhibits Renal Ischemia Reperfusion Injury.Acta histochemica et cytochemica · 2013Article
- Up-regulation of Smurf1 after spinal cord injury in adult rats.Journal of molecular histology · 2013Article
- Resistance to TRAIL in non-transformed cells is due to multiple redundant pathways.Cell death & disease · 2013Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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-alpha, IL-1beta, 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(-/-)) 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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