ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2018
Tissue-type plasminogen activator protects the postsynaptic density in the ischemic brain.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Exercise and fluoxetine in Alzheimer's disease: Molecular mechanisms of synergistic and antagonistic effects (Review).International journal of molecular medicine · 2026Review
- AdipoRon Ameliorates Synaptic Dysfunction and Inhibits tau Hyperphosphorylation through the AdipoR/AMPK/mTOR Pathway in T2DM Mice.Neurochemical research · 2024Article
- Article
- Neuron-targeted Knockout of APE1 Forces Premature Cognitive Impairment and Synaptic Dysfunction in Adult Mice.Aging and disease · 2022Article
- The Role of AMPARs Composition and Trafficking in Synaptic Plasticity and Diseases.Cellular and molecular neurobiology · 2022Review
- Article
- Acupuncture Interventions for Alzheimer's Disease and Vascular Cognitive Disorders: A Review of Mechanisms.Oxidative medicine and cellular longevity · 2022Review
- Review of evidence implicating the plasminogen activator system in blood-brain barrier dysfunction associated with Alzheimer's disease.Ageing and neurodegenerative diseases · 2022Article
- The plasminogen activating system in the pathogenesis of Alzheimer's disease.Neural regeneration research · 2021Review
- Urokinase-Type Plasminogen Activator Protects Cerebral Cortical Neurons from Soluble Aβ-Induced Synaptic Damage.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Urokinase-type plasminogen activator is a modulator of synaptic plasticity in the central nervous system: implications for neurorepair in the ischemic brain.Neural regeneration research · 2020Review
- Urokinase-type plasminogen activator (uPA) regulates the expression and function of growth-associated protein 43 (GAP-43) in the synapse.The Journal of biological chemistry · 2020Article
- Tissue-type plasminogen activator regulates p35-mediated Cdk5 activation in the postsynaptic terminal.Journal of cell science · 2019Article
- Urokinase-type Plasminogen Activator Induces Neurorepair in the Ischemic Brain.Journal of neurology and experimental neuroscience · 2018Article
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Authors and funding
10 authors at 1 institution in 1 country.
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Abstract
Cerebral ischemia causes the presynaptic release of tissue-type plasminogen activator (tPA). The postsynaptic density (PSD) is a postsynaptic structure that provides a matrix where signaling transduction of excitatory synapses takes place. The postsynaptic density protein-95 (PSD-95) is the most abundant scaffolding protein in the postsynaptic density (PSD), where it modulates the postsynaptic response to the presynaptic release of glutamate by regulating the anchoring of glutamate receptors to the PSD. We found that tPA induces the local translation of PSD-95 mRNA and the subsequent recruitment of PSD-95 protein to the PSD, via plasminogen-independent activation of TrkB receptors. Our data show that PSD-95 is removed from the PSD during the early stages of cerebral ischemia, and that this effect is abrogated by either the release of neuronal tPA, or intravenous administration of recombinant tPA (rtPA). We report that the effect of tPA on PSD-95 is associated with inhibition of the phosphorylation and recruitment of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors to the PSD, known to amplify the effect of the excitotoxic injury, and that this is followed by TrkB-mediated protection of dendritic spines from the harmful effects of the hypoxic insult. These data reveal that tPA is a synaptic protector in the ischemic brain.
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