ArticleMolecular medicine reports2015
A disintegrin and metalloprotease 17 promotes microglial cell survival via epidermal growth factor receptor signalling following spinal cord injury.
Article in Molecular medicine reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- Potential Mechanisms Underlying COVID-19-Mediated Central and Peripheral Demyelination: Roles of the RAAS and ADAM-17.Molecular neurobiology · 2025Review
- The Effect of Tissue Inhibitor of Metalloproteinases on Scar Formation after Spinal Cord Injury.Cells · 2024Review
- Role of the prefrontal cortical protease TACE/ADAM17 in neurobehavioral responses to chronic stress during adolescence.Brain and behavior · 2024Article
- Extracellular vesicles epitopes as potential biomarker candidates in patients with traumatic spinal cord injury.Frontiers in immunology · 2024Article
- Effects of Whole-Body Vibration and Manually Assisted Locomotor Therapy on Neurotrophin-3 Expression and Microglia/Macrophage Mobilization Following Thoracic Spinal Cord Injury in Rats.Current issues in molecular biology · 2023Article
- APPlications of amyloid-β precursor protein metabolites in macrocephaly and autism spectrum disorder.Frontiers in molecular neuroscience · 2023Review
- Protein Degradome of Spinal Cord Injury: Biomarkers and Potential Therapeutic Targets.Molecular neurobiology · 2020Review
- Substrate-Specific Activation of α-Secretase by 7-Deoxy-Trans-Dihydronarciclasine Increases Non-Amyloidogenic Processing of β-Amyloid Protein Precursor.Molecules (Basel, Switzerland) · 2020Article
- RNA Sequencing of Peripheral Blood Revealed that the Neurotropic TRK Receptor Signaling Pathway Shows Apparent Correlation in Recovery Following Spinal Cord Injury at Small Cohort.Journal of molecular neuroscience : MN · 2019Article
- Novel Contribution of Secreted Amyloid-β Precursor Protein to White Matter Brain Enlargement in Autism Spectrum Disorder.Frontiers in psychiatry · 2019Review
- Specific inhibition of ADAM17/TACE promotes neurogenesis in the injured motor cortex.Cell death & disease · 2018Article
- The microglial activation profile and associated factors after experimental spinal cord injury in rats.Neuropsychiatric disease and treatment · 2018Article
- The Distinct Role of ADAM17 in APP Proteolysis and Microglial Activation Related to Alzheimer's Disease.Cellular and molecular neurobiology · 2016Review
Corrections and comments
- Retraction · 2024-12-09Author Unresponsive · Concerns/Issues about Data · Concerns/Issues about Article · Duplication of Data · Duplication of/in Article · Euphemisms for Duplication · Investigation by Journal/Publisher ·
- Retracted
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumour necrosis factor-α (TNF-α) converting enzyme (TACE), also termed a disintegrin and metalloprotease 17 (ADAM17), is involved in multiple cell signalling pathways. Through the secretion of epidermal growth factor receptor (EGFR) ligands, ADAM17 can activate the EGFR and is involved in various downstream signalling pathways. The present study aimed to investigate whether ADAM17‑induced EGFR transactivation is involved in microglial cell survival following spinal cord injury (SCI). Reverse transcription quantitative polymerase chain reaction and western blot analysis revealed that ADAM17 was overexpressed in a mouse model following SCI. A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay demonstrated that the viability of human microglia and oligodendrocytes were significantly reduced in a time- and dose-dependent manner following treatment with the ADAM17 antagonist, TNF protease inhibitor 2. Hoechst 33258 staining and flow cytometric analysis revealed that inhibiting ADAM17 increased the rate of cellular apoptosis in neuronal and glial cell cultures, which was accompanied by increased cleavage of caspase-3. Western blot analysis demonstrated that inhibiting ADAM17 resulted in a reduction in the phosphorylation of the EGFR signalling pathway components and thereby impaired functional recovery, inhibited cell viability and prompted microglial apoptosis following SCI. Pre-treatment with the EGFR inhibitor, AG1478, rescued the ADAM17‑mediated proliferation of microglial cells. These data demonstrated that ADAM17 contributed to microglial cell survival, predominantly by EGFR signalling, following SCI.
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Registered trials
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.