ArticleJournal of molecular neuroscience : MN2009
Proteomic analysis of human cerebral endothelial cells activated by glutamate/MK-801: significance in ischemic stroke injury.
Article in Journal of molecular neuroscience : MN, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- Endothelium glutamate receptors in brain pathology.Frontiers in pharmacology · 2025Review
- Neuroprotective effects of cordycepin inhibit glutamate-induced apoptosis in hippocampal neurons.Cell stress & chaperones · 2024Article
- Recovery of Neurovascular Unit Integrity by CDK5-KD Astrocyte Transplantation in a Global Cerebral Ischemia Model.Molecular neurobiology · 2018Article
- Variations in the cerebrospinal fluid proteome following traumatic brain injury and subarachnoid hemorrhage.Pathophysiology : the official journal of the International Society for Pathophysiology · 2017Article
- Major remodeling of brain microvessels during neonatal period in the mouse: A proteomic and transcriptomic study.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Article
- Application of proteomics to cerebrovascular disease.Electrophoresis · 2012Review
- A large-scale electrophoresis- and chromatography-based determination of gene expression profiles in bovine brain capillary endothelial cells after the re-induction of blood-brain barrier properties.Proteome science · 2010Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Glutamate is a major excitatory neurotransmitter in the central nervous system and plays a significant role in the pathophysiology of ischemic stroke. During acute ischemic cerebrovascular disease, glutamate efflux in the CNS produces excitotoxicity in neurons and may mediate forms of stress in other tissues expressing glutamate ionotropic (N-methyl-D-aspartate (NMDA)) receptors, e.g., cerebral endothelial cells. While endothelial cell stress in response to glutamate has been reported (oxidant stress, loss of barrier function), changes in protein expression produced by glutamate (an agonist of metabotropic and NMDA receptors) have not been documented. Here, we have examined how exposure of human cerebral endothelial cells to glutamate, in the presence and absence of the NMDA receptor antagonist MK-801, can alter the proteomic profile of cerebral endothelial cells. We found several important changes in the proteins expressed by cerebral endothelial cells in response to glutamate. Interestingly, MK-801 itself had some direct effects on cerebral endothelial cells. Taken together, our findings demonstrate that cerebral endothelial cells respond to glutamate by altering their protein expression profile. We assume that protein alterations found in the cerebral endothelial proteome, in response to glutamate and which were blocked by MK-801, may be important vascular targets in better understanding the pathogenesis of ischemic stroke.
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Registered trials
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