ArticleCell death & disease2013
ADAM17 is a survival factor for microglial cells in vitro and in vivo after spinal cord injury in mice.
Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- Necroptosis is a key contributor to impaired cardiac repair following myocardial infarction.Cell death & disease · 2026Article
- Quantum mechanics-based multitensor AI/ML uniquely able to discover, validate, and interpret predictors from small-cohort noisy high-dimensional multiomic data.APL quantum · 2026Article
- Impact of PKC-MAPK Signaling on Cardiac Sympathetic Overactivation in Type-2 Diabetes Mellitus.International journal of molecular sciences · 2026Article
- Proinflammatory microglial activation impairs in vitro cortical tissue repair via zinc-dependent ADAM17 cleavage of the CSF-1 receptor.Journal of neurochemistry · 2025Article
- Potential Mechanisms Underlying COVID-19-Mediated Central and Peripheral Demyelination: Roles of the RAAS and ADAM-17.Molecular neurobiology · 2025Review
- 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
- Immune Responses to IAV Infection and the Roles of L-Selectin and ADAM17 in Lymphocyte Homing.Pathogens (Basel, Switzerland) · 2022Review
- Expression of SARS-CoV-2-related receptors in cells of the neurovascular unit: implications for HIV-1 infection.Journal of neuroinflammation · 2021Article
- Expression of SARS-CoV-2-related Receptors in Cells of the Neurovascular Unit: Implications for HIV-1 Infection.Research square · 2021Article
- Article
- HDAC8 Inhibition Reduces Lesional Iba-1+ Cell Infiltration after Spinal Cord Injury without Effects on Functional Recovery.International journal of molecular sciences · 2020Article
- Reappraisal of Human HOG and MO3.13 Cell Lines as a Model to Study Oligodendrocyte Functioning.Cells · 2019Article
- Matrix metalloproteinases and ADAMs in stroke.Cellular and molecular life sciences : CMLS · 2019Review
- MicroRNA-23b attenuates the HInternational journal of clinical and experimental pathology · 2018Article
- Analysis of the Role of CX3CL1 (Fractalkine) and Its Receptor CX3CR1 in Traumatic Brain and Spinal Cord Injury: Insight into Recent Advances in Actions of Neurochemokine Agents.Molecular neurobiology · 2017Review
- Cell-Based Delivery of Interleukin-13 Directs Alternative Activation of Macrophages Resulting in Improved Functional Outcome after Spinal Cord Injury.Stem cell reports · 2016Article
- Interleukin-25 is detrimental for recovery after spinal cord injury in mice.Journal of neuroinflammation · 2016Article
- Necroptosis, a novel type of programmed cell death, contributes to early neural cells damage after spinal cord injury in adult mice.The journal of spinal cord medicine · 2015Article
- A disintegrin and metalloprotease 17 promotes microglial cell survival via epidermal growth factor receptor signalling following spinal cord injury.Molecular medicine reports · 2015Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A disintegrin and metalloprotease 17 (ADAM17) is a sheddase with important substrates including tumor necrosis factor-α (TNF-α) and its receptors, the p75 neurotrophin receptor (p75NTR), and members of the epidermal growth factor family. The rationale of this study was to inhibit ADAM17-induced shedding of soluble TNF-α in order to reduce detrimental inflammation after spinal cord injury (SCI). However, using the specific ADAM17 blocker BMS-561392 in neuronal and glial cell cultures, we show that proper functioning of ADAM17 is vital for oligodendrocyte and microglia survival in a p44 MAPK-dependent manner. In contrast, genetic ablation of ADAM17 specifically increases microglial death. Surprisingly, although blocking ADAM17 in vivo does not substantially change the ratio between membrane-bound and soluble TNF-α, it increases expression of the pro-apoptotic marker Bax and microglial apoptosis while impairing functional recovery after SCI. These data suggest that ADAM17 is a key survival factor for microglial cells after 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.