ArticleMolecular neurobiology2013
Matrix metalloproteinase-2 and metalloproteinase-9 activities are associated with blood-brain barrier dysfunction in an animal model of severe sepsis.
Article in Molecular neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 2 of them syntheses that pooled it.
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Who cites it
72 citing papers in PubMed, 2 syntheses or guidelines pooled it, 121 citations in OpenAlex.
- The Key Drivers of Brain Injury by Systemic Inflammatory Responses after Sepsis: Microglia and Neuroinflammation.Molecular neurobiology · 2023Pooled it
- Long-Term Cognitive Outcomes After Sepsis: a Translational Systematic Review.Molecular neurobiology · 2019Pooled it
- Role of Matrix Metalloproteinases and Tissue Inhibitors in Sepsis Pathogenesis.Medical sciences (Basel, Switzerland) · 2026Article
- Hippocampal cytopathology orchestrates post-septic cognitive dysfunction.Metabolic brain disease · 2026Review
- Mitochondrial dysfunction in neonatal brain injury: from molecular mechanisms to therapeutic interventions.Journal of translational medicine · 2026Review
- Review
- Effects of Treatment with Dexmedetomidine on Neurochemical and Cognitive Alterations Induced by Sepsis in an Animal Model.Journal of molecular neuroscience : MN · 2025Article
- Unraveling the Vicious Cycle: Oxidative Stress and Neurotoxicity in Neurodegenerative Diseases.FASEB bioAdvances · 2025Review
- Convergence of sepsis-associated encephalopathy pathogenesis onto microglia.Journal of translational medicine · 2025Review
- Sepsis-associated encephalopathy: Mechanisms, Diagnosis, and Treatments update.International journal of biological sciences · 2025Review
- Plasma brain-related biomarkers and potential therapeutic targets in pediatric ECMO.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Visualization of Blood-Brain Barrier Disruption in Septic Mice with the New Method Based on in Vivo Imaging Technology.Neurocritical care · 2024Article
- Exploring molecular mechanisms of postoperative delirium through multi-omics strategies in plasma exosomes.Scientific reports · 2024Article
- Maresin-1 Ameliorates Sepsis-Induced Microglial Activation Through Modulation of the P38 MAPK Pathway.Neurochemical research · 2024Article
- Lung-brain crosstalk: Behavioral disorders and neuroinflammation in septic survivor mice.Brain, behavior, & immunity - health · 2024Article
- Targeted rescue of synaptic plasticity improves cognitive decline in sepsis-associated encephalopathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Obesity-induced blood-brain barrier dysfunction: phenotypes and mechanisms.Journal of neuroinflammation · 2024Review
- Treatment with an inhibitor of matrix metalloproteinase 9 or cathepsin K lengthens embryonic lower jaw bone.Orthodontics & craniofacial research · 2023Article
- Neurochemical effects of sepsis on the brain.Clinical science (London, England : 1979) · 2023Article
- Mechanism of Action of Natural Compounds in Peripheral Multiorgan Dysfunction and Hippocampal Neuroinflammation Induced by Sepsis.Antioxidants (Basel, Switzerland) · 2023Article
12 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is no description on the mechanisms associated with blood-brain barrier (BBB) disruption during sepsis development. Thus, we here determined changes in permeability of the BBB in an animal model of severe sepsis and the role of matrix metalloproteinase (MMP)-2 and MMP-9 in the dysfunction of the BBB. Sepsis was induced in Wistar rats by cecal ligation and perforation. BBB permeability was assessed using the Evans blue dye method. The content of MMP-2 and MMP-9 in the cerebral microvessels was determined by western blot. The activity of MMP-2 and MMP-9 was determined using zymography. An inhibitor of MMP-2 and MMP-9 or specific inhibitors of MMP-2 or MMP-9 were administered to define the role of MMPs on BBB permeability, brain inflammatory response, and sepsis-induced cognitive alterations. The increase of BBB permeability is time-related to the increase of MMP-9 and MMP-2 in the microvessels, both in cortex and hippocampus. Using an MMP-2 and MMP-9 inhibitor, or specific MMP-2 or MMP-9 inhibitors, the increase in the permeability of the BBB was reversed. This was associated with lower brain levels of interleukin (IL)-6 and lower oxidative damage. In contrast, only the inhibition of both MMP-9 and MMP-2 was able to improve acute cognitive alterations associated with sepsis. In conclusion, MMP-2 and MMP-9 activation seems to be a major step in BBB dysfunction, but BBB dysfunction seems not to be associated with acute cognitive dysfunction during sepsis development.
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