ArticleNeurochemical research2016
Upregulation of PSMB4 is Associated with the Necroptosis after Spinal Cord Injury.
Article in Neurochemical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Different Ways to Die: Cell Death Pathways and Their Association With Spinal Cord Injury.Neurospine · 2023Article
- Outcomes of RIP Kinase Signaling During Neuroinvasive Viral Infection.Current topics in microbiology and immunology · 2023Review
- Cellular PSMB4 Protein Suppresses Influenza A Virus Replication through Targeting NS1 Protein.Viruses · 2022Article
- Programmed cell death in spinal cord injury pathogenesis and therapy.Cell proliferation · 2021Review
- Comparative Morphometry of the Wisconsin Miniature SwineAnnals of neurosciences · 2018Article
- Necroptosis: a regulated inflammatory mode of cell death.Journal of neuroinflammation · 2018Review
- The Role of Smurf1 in Neuronal Necroptosis after Lipopolysaccharide-Induced Neuroinflammation.Cellular and molecular neurobiology · 2018Article
- The Pathogenesis of Necroptosis-Dependent Signaling Pathway in Cerebral Ischemic Disease.Behavioural neurology · 2018Review
- The Contribution of Necroptosis in Neurodegenerative Diseases.Neurochemical research · 2017Review
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal cord injury (SCI) is one of the most common and severe complications in spine injury. It is difficult to prevent cell necroptosis and promote the survival of residual neurons after SCI. Proteasome beta-4 subunit (PSMB4) is the first proteasomal subunit with oncogenic properties promoting cancer cell survival and tumor growth in vivo, and our previous study showed that PSMB4 is significantly associated with neuronal apoptosis in neuroinflammation. However, PSMB4 function in the necroptosis after SCI is unkown. RIP3, a key regulatory factor of necroptosis, correlates with the induction of necroptosis in various types of cells and signaling pathway. Upregulation of the RIP3 expression may play a role as a novel molecular mechanism in secondary neural tissue damage following SCI. In this study, we established an acute spinal cord contusion injury model in adult rats to investigate the potential role of PSMB4 during the pathological process of SCI. We found PSMB4 expression was significantly up-regulated 3 days after injury by western blot and immunohistochemical staining. Double immunofluorescent staining indicated obvious changes of PSMB4 expression occurred in neurons. Significant up-regulation of PSMB4 expression was observed in Rip3 positive neurons at 3 days after SCI, which indicated that PSMB4 might play a vital role in the regulation of Rip3. Overexpress and knockdown PSMB4 could intervene the RIP3 and Mixed lineage kinase domain-like protein (MLKL) pathway in Tumor necrosis factor-α (TNF-α) induced necroptosis cell model. Based on our experimental data, we boldly conclude that PSMB4 is associated with RIP3 involved necroptosis after SCI.
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