Please use this identifier to cite or link to this item: 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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