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https://doi.org/10.1186/2040-7378-6-7
Title: | Intravenous immunoglobulin (IVIg) provides protection against endothelial cell dysfunction and death in ischemic stroke | Authors: | Widiapradja, A Santro, T Basta, M Sobey, C.G Manzanero, S Arumugam, T.V |
Keywords: | apoptosis inducing factor claudin 5 immunoglobulin immunoglobulin G junctional adhesion molecule A neuroprotective agent occludin protein bcl 2 protein bcl xl tight junction protein animal cell animal experiment animal model article blood brain barrier brain ischemia cell damage cell death cell protection continuous infusion controlled study down regulation endothelium cell flow cytometry fluorescence microscope immunoblotting immunocompetent cell immunocytochemistry in vivo study lymphocytic infiltration male mouse neuromodulation neuroprotection nonhuman oxygen and glucose deprivation priority journal procedures concerning cells protein expression |
Issue Date: | 2014 | Publisher: | BioMed Central Ltd. | Citation: | Widiapradja, A, Santro, T, Basta, M, Sobey, C.G, Manzanero, S, Arumugam, T.V (2014). Intravenous immunoglobulin (IVIg) provides protection against endothelial cell dysfunction and death in ischemic stroke. Experimental and Translational Stroke Medicine 6 (1) : 7. ScholarBank@NUS Repository. https://doi.org/10.1186/2040-7378-6-7 | Abstract: | Background: The brain endothelium is a key component of the blood brain barrier which is compromised following ischemia, allowing infiltration of damaging immune cells and other inflammatory molecules into the brain. Intravenous immunoglobulin (IVIg) is known to reduce infarct size in a mouse model of experimental stroke.Findings: Flow cytometry analysis showed that the protective effect of IVIg in ischemia and reperfusion injury in vivo is associated with reduced leukocyte infiltration, suggesting an involvement of the endothelium. In an in vitro model of ischemia, permeability analysis of the mouse brain endothelial cell line bEnd.3 revealed that IVIg prevented the loss of permeability caused by oxygen and glucose deprivation (OGD). In addition, western blot analysis of these brain endothelial cells showed that IVIg prevented the down-regulation of tight junction proteins claudin 5 and occludin and the decline in anti-apoptotic proteins Bcl-2 and Bcl-XL caused by OGD.Conclusion: IVIg protects endothelial cells from ischemic insult. These studies support the use of IVIg as a pharmacological intervention for stroke therapy. © 2014 Widiapradja et al.; licensee BioMed Central Ltd. | Source Title: | Experimental and Translational Stroke Medicine | URI: | https://scholarbank.nus.edu.sg/handle/10635/175538 | ISSN: | 20407378 | DOI: | 10.1186/2040-7378-6-7 |
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