ArticleMolecular neurobiology2018
Elevation of MMP-9 Levels Promotes Epileptogenesis After Traumatic Brain Injury.
Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 68 citations in OpenAlex.
- Antiepileptic and antiepileptogenic effects ofIBRO neuroscience reports · 2026Article
- Profiling of hypoxic and extracellular matrix remodeling markers in biofluids and cerebral tissue after traumatic brain injury: expression and signaling crosstalk of HIF-1α, MMP-9/14 and EPHA2.International journal of legal medicine · 2026Article
- Neuronal toll-like receptor-4 regulation of matrix metalloproteinase-9 activity mediates dentate circuit dysfunction after traumatic brain injury.Journal of neuroinflammation · 2026Article
- Neuronal Toll-like Receptor-4 regulation of Matrix Metalloproteinase-9 Activity Mediates Dentate Circuit Dysfunction after Traumatic Brain Injury.bioRxiv : the preprint server for biology · 2026Article
- Extracellular matrix and perineuronal nets in neural plasticity, memory, and epileptogenesis.Frontiers in molecular neuroscience · 2026Review
- Article
- Development and Characterization of Hyaluronic Acid Microgels for Neural Regeneration Applications.Journal of biomedical materials research. Part A · 2025Article
- The link between impact-induced tensile strain and dendritic spine morphology in porcine brain tissue.PloS one · 2025Article
- Inflammatory proteins as acute biomarkers of post-traumatic epilepsy.Frontiers in neurology · 2025Article
- Viral-mediated increased hippocampal neurogranin modulate synapses at one month in a rat model of controlled cortical impact.Scientific reports · 2024Article
- Review
- From spreading depolarization to blood-brain barrier dysfunction: navigating traumatic brain injury for novel diagnosis and therapy.Nature reviews. Neurology · 2024Review
- Increased expression of chondroitin sulfate proteoglycans in dentate gyrus and amygdala causes postinfectious seizures.Brain : a journal of neurology · 2024Article
- Matrix Metalloproteinase-9 Contributes to Epilepsy Development after Ischemic Stroke in Mice.International journal of molecular sciences · 2024Article
- Synthesis and Characterization of a Novel Concentration-Independent Fluorescent Chloride Indicator, ABP-Dextran, Optimized for Extracellular Chloride Measurement.Biomolecules · 2024Article
- Meta-analysis of MMP-9 levels in the serum of patients with epilepsy.Frontiers in neuroscience · 2024Review
- Effects of metformin on parasitological, pathological changes in the brain and liver and immunological aspects during visceral toxocariasis in mice.Parasitology research · 2023Article
- An Activity-Based Nanosensor for Minimally-Invasive Measurement of Protease Activity in Traumatic Brain Injury.Advanced functional materials · 2023Article
- Infection-induced epilepsy is caused by increased expression of chondroitin sulfate proteoglycans in hippocampus and amygdala.bioRxiv : the preprint server for biology · 2023Article
- Antidiabetic Drugs Can Reduce the Harmful Impact of Chronic Smoking on Post-Traumatic Brain Injuries.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 4 countries.
Funding
Abstract
Posttraumatic epilepsy (PTE) is a recurrent seizure disorder that often develops secondary to traumatic brain injury (TBI) that is caused by an external mechanical force. Recent evidence shows that the brain extracellular matrix plays a major role in the remodeling of neuronal connections after injury. One of the proteases that is presumably responsible for this process is matrix metalloproteinase-9 (MMP-9). The levels of MMP-9 are elevated in rodent brain tissue and human blood samples after TBI. However, no studies have described the influence of MMP-9 on the development of PTE. The present study used controlled cortical impact (CCI) as a mouse model of TBI. We examined the detailed kinetics of MMP-9 levels for 1 month after TBI and observed two peaks after injury (30 min and 6 h after injury). We tested the hypothesis that high levels of MMP-9 predispose individuals to the development of PTE, and MMP-9 inhibition would protect against PTE. We used transgenic animals with either MMP-9 knockout or MMP-9 overexpression. MMP-9 overexpression increased the number of mice that exhibited TBI-induced spontaneous seizures, and MMP-9 knockout decreased the appearance of seizures. We also evaluated changes in responsiveness to a single dose of the chemoconvulsant pentylenetetrazol. MMP-9-overexpressing mice exhibited a significantly shorter latency between pentylenetetrazol administration and the first epileptiform spike. MMP-9 knockout mice exhibited the opposite response profile. Finally, we found that the occurrence of PTE was correlated with the size of the lesion after injury. Overall, our data emphasize the contribution of MMP-9 to TBI-induced structural and physiological alterations in brain circuitry that may lead to the development of PTE.
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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.