ArticleBMC neuroscience2015
Upregulation of the receptor-interacting protein 3 expression and involvement in neural tissue damage after spinal cord injury in mice.
Article in BMC neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Repurposing Dexmedetomidine: Early Pharmacological Hypothermia Enhances Neuroprotection and Improves Locomotor and Bladder Functional Recovery after Spinal Cord Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- RIP1 inhibition protects retinal ganglion cells in glaucoma models of ocular injury.Cell death and differentiation · 2025Article
- Therapeutic effects of exendin-4 on spinal cord injury via restoring autophagy function and decreasing necroptosis in neuron.CNS neuroscience & therapeutics · 2024Article
- Human Spinal Oligodendrogenic Neural Progenitor Cells Enhance Pathophysiological Outcomes and Functional Recovery in a Clinically Relevant Cervical Spinal Cord Injury Rat Model.Stem cells translational medicine · 2023Article
- Outcomes of RIP Kinase Signaling During Neuroinvasive Viral Infection.Current topics in microbiology and immunology · 2023Review
- Receptor-Interacting Protein Kinase 3 Inhibition Relieves Mechanical Allodynia and Suppresses NLRP3 Inflammasome and NF-κB in a Rat Model of Spinal Cord Injury.Frontiers in molecular neuroscience · 2022Article
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- Genetic inactivation of RIP1 kinase does not ameliorate disease in a mouse model of ALS.Cell death and differentiation · 2021Article
- Experimental infection of hepatitis E virus induces pancreatic necroptosis in miniature pigs.Scientific reports · 2020Article
- The Lipoxin A4 Receptor Agonist BML-111 Alleviates Inflammatory Injury and Oxidative Stress in Spinal Cord Injury.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- B-RAFCells · 2019Article
- Neuronal Cell Death.Physiological reviews · 2018Review
- Inhibiting RIPK1 Limits Neuroinflammation and Alleviates Postoperative Cognitive Impairments in D-Galactose-Induced Aged Mice.Frontiers in behavioral neuroscience · 2018Article
- Necrostatin-1 Mitigates Endoplasmic Reticulum Stress After Spinal Cord Injury.Neurochemical research · 2017Article
- Necrostatin-1 attenuates early brain injury after subarachnoid hemorrhage in rats by inhibiting necroptosis.Neuropsychiatric disease and treatment · 2017Article
- Upregulation of PSMB4 is Associated with the Necroptosis after Spinal Cord Injury.Neurochemical research · 2016Article
- Deletion ofeNeuroArticle
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNecroptosis is a newly identified type of programmed cell death that differs from apoptosis. Recent studies have demonstrated that necroptosis is involved in multiple pathologies of various human diseases. Receptor-interacting protein 3 (RIP3) is known to be a critical regulator of necroptosis. This study investigated alterations in the RIP3 expression and the involvement in neural tissue damage after spinal cord injury (SCI) in mice.
resultsImmunohistochemical analysis demonstrated that the RIP3 expression was significantly increased in the lesion site after spinal cord hemisection. The increased expression of RIP3 started at 24 h, peaked at 3 days and lasted for at least 21 days after hemisection. The RIP3 expression was observed in neurons, astrocytes and oligodendrocytes. Western blot analysis also demonstrated the RIP3 protein expression significantly upregulated in the injured spinal cord. RIP3 staining using propidium iodide (PI)-labeled sections showed most of the PI-labeled cells were observed as RIP3-positive. Double staining of TUNEL and RIP3 demonstrated that TUNEL-positive cells exhibiting shrunken or fragmented nuclei, as generally observed in apoptotic cells, rarely expressed RIP3.
conclusionsThe present study first demonstrated that the expression of RIP3 is dramatically upregulated in various neural cells in the injured spinal cord and peaked at 3 days after injury. Additionally, most of the PI-labeled cells expressed RIP3 in response to neural tissue damage after SCI. The present study suggested that the upregulation of the RIP3 expression may play a role as a novel molecular mechanism in secondary neural tissue damage following SCI. However, further study is needed to clarify the specific molecular mechanism underlying the relationship between the RIP3 expression and cell death in the injured spinal cord.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.