ArticleCellular and molecular neurobiology2007
Adverse effect of cyclosporin A on barrier functions of cerebral microvascular endothelial cells after hypoxia-reoxygenation damage in vitro.
Article in Cellular and molecular neurobiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
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- Reactive oxygen species contribute to delirium-like behavior by activating CypA/MMP9 signaling and inducing blood-brain barrier impairment in aged mice following anesthesia and surgery.Frontiers in aging neuroscience · 2022Article
- iPS Cell Differentiation into Brain Microvascular Endothelial Cells.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Role of pericyte-derived SENP1 in neuronal injury after brain ischemia.CNS neuroscience & therapeutics · 2020Article
- Posterior Reversible Encephalopathy Syndrome After Transplantation: a Review.Molecular neurobiology · 2016Review
- Central modulation of cyclosporine-induced hypertension.Naunyn-Schmiedeberg's archives of pharmacology · 2015Review
- Multiple sphingolipid abnormalities following cerebral microendothelial hypoxia.Journal of neurochemistry · 2014Article
- Differential microRNA profiling in a cellular hypoxia reoxygenation model upon posthypoxic propofol treatment reveals alterations in autophagy signaling network.Oxidative medicine and cellular longevity · 2013Article
- Article
- Recovery of motor spontaneous activity after intranasal delivery of human recombinant erythropoietin in a focal brain hypoxia model induced by CoCl2 in rats.Neurotoxicity research · 2011Article
- Experimental models for assaying microvascular endothelial cell pathophysiology in stroke.Molecules (Basel, Switzerland) · 2010Review
- Interleukin-25 expressed by brain capillary endothelial cells maintains blood-brain barrier function in a protein kinase Cepsilon-dependent manner.The Journal of biological chemistry · 2009Article
- Tissue plasminogen activator enhances the hypoxia/reoxygenation-induced impairment of the blood-brain barrier in a primary culture of rat brain endothelial cells.Cellular and molecular neurobiology · 2008Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypoxia and post-hypoxic reoxygenation induces disruption of the blood-brain barrier (BBB). Alterations of the BBB function after hypoxia/reoxygenation (H/R) injury remain unclear. Cyclosporin A (CsA), a potent immunosuppressant, induces neurotoxic effects by entering the brain, although the transport of CsA across the BBB is restricted by P-glycoprotein (P-gp), a multidrug efflux pump, and tight junctions of the brain capillary endothelial cells. The aim of this study was to evaluate whether the BBB after H/R damage is vulnerable to CsA-induced BBB dysfunction. We attempted to establish a pathophysiological BBB model with immortalized mouse brain capillary endothelial (MBEC4) cells. The effects of CsA on permeability and P-gp activity of the MBEC4 cells were then examined. Exposure to hypoxia for 4 h and reoxygenation for 1 h (H/R (4 h/1 h)) produced a significant decrease in P-gp function of MBEC4 cells, without changing cell viability and permeability for sodium fluorescein and Evan's blue-albumin at 7 days after H/R (4 h/1 h). CsA-induced hyperpermeability and P-gp dysfunction in MBEC4 monolayers at 7 days after H/R (4 h/1 h) were exacerbated. The possibility that CsA penetrates the BBB with incomplete functions in the vicinity of cerebral infarcts to induce neurotoxicity has to be considered.
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