ArticleMetabolic brain disease2015
Ablation of matrix metalloproteinase-9 gene decreases cerebrovascular permeability and fibrinogen deposition post traumatic brain injury in mice.
Article in Metabolic brain disease, 2015. 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, 67 citations in OpenAlex.
- Targeting inflammation and coagulation: MMP-9 deficiency exacerbates sepsis induced acute lung injury through fibrinogen-driven inflammation.Respiratory research · 2026Article
- Blood-brain barrier disruption: a pervasive driver and mechanistic link between traumatic brain injury and Alzheimer's disease.Translational neurodegeneration · 2025Review
- Fibrinogen and Neuroinflammation in the Neurovascular Unit in Stroke.Journal of inflammation research · 2025Review
- From spreading depolarization to blood-brain barrier dysfunction: navigating traumatic brain injury for novel diagnosis and therapy.Nature reviews. Neurology · 2024Review
- Detrimental Roles of Hypoxia-Inducible Factor-1α in Severe Hypoxic Brain Diseases.International journal of molecular sciences · 2024Review
- The Effect of Reduced Fibrinogen on Cerebrovascular Permeability during Traumatic Brain Injury in Fibrinogen Gene Heterozygous Knockout Mice.Biomolecules · 2024Article
- ICAM-1 Deletion Using CRISPR/Cas9 Protects the Brain from Traumatic Brain Injury-Induced Inflammatory Leukocyte Adhesion and Transmigration Cascades by Attenuating the Paxillin/FAK-Dependent Rho GTPase Pathway.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Overexpression of endothelial S1pr2 promotes blood-brain barrier disruption via JNK/c-Jun/MMP-9 pathway after traumatic brain injury in bothFrontiers in pharmacology · 2024Article
- Fibrinogen Inhibits Metalloproteinase-9 Activation and Syndecan-1 Cleavage to Protect Lung Function in ApoE Null Mice After Hemorrhagic Shock.The Journal of surgical research · 2023Article
- Role of neutrophils in different stages of atherosclerosis.Innate immunity · 2023Review
- Imbalance of Essential Metals in Traumatic Brain Injury and Its Possible Link with Disorders of Consciousness.International journal of molecular sciences · 2023Review
- Vascular Effects on Cerebrovascular Permeability and Neurodegeneration.Biomolecules · 2023Review
- Neutrophil extracellular traps mediate deep vein thrombosis: from mechanism to therapy.Frontiers in immunology · 2023Review
- The Role of Nuclear Factor-Kappa B in Fibrinogen-Induced Inflammatory Responses in Cultured Primary Neurons.Biomolecules · 2022Article
- Review
- Tissue factor release following traumatic brain injury drives thrombin generation.Research and practice in thrombosis and haemostasis · 2022Article
- Role of Bevacizumab on Vascular Endothelial Growth Factor in Apolipoprotein E Deficient Mice after Traumatic Brain Injury.International journal of molecular sciences · 2022Article
- NS1619 Alleviate Brain-Derived Extracellular Vesicle-Induced Brain Injury by Regulating BKca Channel and Nrf2/HO-1/NF-ĸB Pathway.Oxidative medicine and cellular longevity · 2022Article
- Blood-Brain Barrier Mechanisms in Stroke and Trauma.Handbook of experimental pharmacology · 2022Review
- Platelet-like particles reduce coagulopathy-related and neuroinflammatory pathologies post-experimental traumatic brain injury.Journal of biomedical materials research. Part B, Applied biomaterials · 2021Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) is accompanied with enhanced matrix metalloproteinase-9 (MMP-9) activity and elevated levels of plasma fibrinogen (Fg), which is a known inflammatory agent. Activation of MMP-9 and increase in blood content of Fg (i.e. hyperfibrinogenemia, HFg) both contribute to cerebrovascular disorders leading to blood brain barrier disruption. It is well-known that activation of MMP-9 contributes to vascular permeability. It has been shown that at an elevated level (i.e. HFg) Fg disrupts blood brain barrier. However, mechanisms of their actions during TBI are not known. Mild TBI was induced in wild type (WT, C57BL/6 J) and MMP-9 gene knockout (Mmp9(-/-)) homozygous, mice. Pial venular permeability to fluorescein isothiocyanate-conjugated bovine serum albumin in pericontusional area was observed 14 days after injury. Mice memory was tested with a novel object recognition test. Increased expression of Fg endothelial receptor intercellular adhesion protein-1 and formation of caveolae were associated with enhanced activity of MMP-9 causing an increase in pial venular permeability. As a result, an enhanced deposition of Fg and cellular prion protein (PrP(C)) were found in pericontusional area. These changes were attenuated in Mmp9(-/-) mice and were associated with lesser loss of short-term memory in these mice than in WT mice. Our data suggest that mild TBI-induced increased cerebrovascular permeability enhances deposition of Fg-PrP(C) and loss of memory, which is ameliorated in the absence of MMP-9 activity. Thus, targeting MMP-9 activity and blood level of Fg can be a possible therapeutic remedy to diminish vasculo-neuronal damage after TBI.
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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.