ArticleCell death & disease2018
Specific inhibition of ADAM17/TACE promotes neurogenesis in the injured motor cortex.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Sex-Specific Neurogenic and Cognitive Responses in a Murine Model of Accelerated Aging.Aging cell · 2026Article
- ErbB signaling in brain injury regeneration: Pathway interactions and therapeutic potential.Neural regeneration research · 2026Article
- The subventricular zone neurogenic niche provides adult born functional neurons to repair cortical brain injuries in response to diterpenoid therapy.Stem cell research & therapy · 2025Article
- Targeting epidermal growth factor receptor to recruit newly generated neuroblasts in cortical brain injuries.Journal of translational medicine · 2023Article
- Mini-Review: Role of Drugs Affecting Renin-Angiotensin System (RAS) in Traumatic Brain Injury (TBI): What We Know and What We Should Know.Korean journal of neurotrauma · 2023Review
- Rescue of neurogenesis and age-associated cognitive decline in SAMP8 mouse: Role of transforming growth factor-alpha.Aging cell · 2023Article
- Migratory Response of Cells in Neurogenic Niches to Neuronal Death: The Onset of Harmonic Repair?International journal of molecular sciences · 2023Review
- SARS-CoV-2 and Hypertension: Evidence Supporting Invasion into the Brain Via Baroreflex Circuitry and the Role of Imbalanced Renin-Angiotensin-Aldosterone-System.Neuroscience insights · 2023Article
- Novel structured ADAM17 small-molecule inhibitor represses ADAM17/Notch pathway activation and the NSCLC cells' resistance to anti-tumour drugs.Frontiers in pharmacology · 2023Article
- Radial glia and radial glia-like cells: Their role in neurogenesis and regeneration.Frontiers in neuroscience · 2022Review
- Article
- Effects of classical PKC activation on hippocampal neurogenesis and cognitive performance: mechanism of action.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021Article
- Strategies to Target ADAM17 in Disease: From its Discovery to the iRhom Revolution.Molecules (Basel, Switzerland) · 2021Review
- A novel PKC activating molecule promotes neuroblast differentiation and delivery of newborn neurons in brain injuries.Cell death & disease · 2020Article
- MicroalgaeFrontiers in cell and developmental biology · 2020Article
- Tissue Engineering and Biomaterial Strategies to Elicit Endogenous Neuronal Replacement in the Brain.Frontiers in neurology · 2020Review
- ADAM17/TACE: a key molecule in brain injury regeneration.Neural regeneration research · 2019Article
- Protein Kinase C: Targets to Regenerate Brain Injuries?Frontiers in cell and developmental biology · 2019Article
- Protein Kinase C Inhibition Mediates Neuroblast Enrichment in Mechanical Brain Injuries.Frontiers in cellular neuroscience · 2018Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain injuries in the adult mammalian brain are accompanied by a fast neurogenic response inside neurogenic niches. However, this response does not contribute to the generation of new neurons within damaged tissues like the cerebral cortex, which are essentially non-neurogenic. This occurs because injuries create a hostile environment that favors gliogenesis. Overexpression and sequential activation of the ADAM17/TGFα/EGFR signaling cascade are crucial for the generation of this gliogenic/non-neurogenic environment. Here, we demonstrate that chronic local infusion of a general metalloprotease inhibitor in areas of traumatic cortical injury in adult mice moderately increased the number of neuroblasts around the lesion, by facilitating the survival of neuroblasts and undifferentiated progenitors, which had migrated to the perilesional area from the subventricular zone. Next, we generated a dominant-negative version of ADAM17 metalloprotease, consisting of a truncated protein containing only the pro-domain (ADAM17-Pro). Specific inhibition of ADAM17 activity by ADAM17-Pro overexpression increased the generation of new neurons in vitro. Local overexpression of ADAM17-Pro in injured cortex in vivo, mediated by lentiviral vectors, dramatically increased the number of neuroblasts observed at the lesion 14 days after injury. Those neuroblasts were able to differentiate into cholinergic and GABAergic neurons 28 days after injury. We conclude that ADAM17 is a putative target to develop new therapeutic tools for the treatment of traumatic brain injury.
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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.