ArticleNeural regeneration research2019
Expression and localization of absent in melanoma 2 in the injured spinal cord.
Article in Neural regeneration research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Integrated Multi-Omics Analysis Reveals IRF1-Driven Microglial PANoptosis via ZBP1 in Spinal Cord Injury.Journal of inflammation research · 2026Article
- Mechanisms of Traumatic Spinal Cord Injury AIS Grade Conversion.Neurotrauma reports · 2025Review
- AIM2 promotes excitatory glutamate receptor expression by inhibiting STING and contributes to bone cancer pain in male mice.Scientific reports · 2024Article
- Constituents fromMolecules (Basel, Switzerland) · 2024Article
- Cytosolic DNA sensors in neurodegenerative diseases: from physiological defenders to pathological culprits.EMBO molecular medicine · 2024Review
- The roles of AIM2 in neurodegenerative diseases: insights and therapeutic implications.Frontiers in immunology · 2024Review
- The Role of Gasdermin-D-Mediated Pyroptosis in Organ Injury and Its Therapeutic Implications.Organogenesis · 2023Review
- An emerging role of inflammasomes in spinal cord injury and spinal cord tumor.Frontiers in immunology · 2023Review
- Role of pyroptosis in spinal cord injury and its therapeutic implications.Journal of advanced research · 2021Review
- Gonadal Hormones E2 and P Mitigate Cerebral Ischemia-Induced Upregulation of the AIM2 and NLRC4 Inflammasomes in Rats.International journal of molecular sciences · 2020Article
- Type I interferon (IFN)-inducible Absent in Melanoma 2 proteins in neuroinflammation: implications for Alzheimer's disease.Journal of neuroinflammation · 2019Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In traumatic brain injury, absent in melanoma 2 (AIM2) has been demonstrated to be involved in pyroptotic neuronal cell death. Although the pathophysiological mechanism of spinal cord injury is similar to that of brain injury, the expression and cellular localization of AIM2 after spinal cord injury is still not very clear. In the present study, we used a rat model of T9 spinal cord contusive injury, produced using the weight drop method. The rats were randomly divided into 1-hour, 6-hour, 1-day, 3-day and 6-day (post-injury time points) groups. Sham-operated rats only received laminectomy at T9 without contusive injury. Western blot assay revealed that the expression levels of AIM2 were not significantly different among the 1-hour, 6-hour and 1-day groups. The expression levels of AIM2 were markedly higher in the 1-hour, 6-hour and 1-day groups compared with the sham, 3-day and 7-day groups. Double immunofluorescence staining demonstrated that AIM2 was expressed by NeuN
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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.