2014
DOI: 10.1007/s12035-014-8973-5
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Acetyl-L-Carnitine Prevents Methamphetamine-Induced Structural Damage on Endothelial Cells via ILK-Related MMP-9 Activity

Abstract: Methamphetamine (METH) is a potent psychostimulant highly used worldwide. Recent studies evidenced the involvement of METH in the breakdown of the blood-brain-barrier (BBB) integrity leading to compromised function. The involvement of the matrix metalloproteinases (MMPs) in the degradation of the neurovascular matrix components and tight junctions (TJs) is one of the most recent findings in METH-induced toxicity. As BBB dysfunction is a pathological feature of many neurological conditions, unveiling new protec… Show more

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Cited by 29 publications
(26 citation statements)
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“…Previous studies showed that METH impacts actin filaments, leading to actin depolymerization, altered cell shape and local accumulation of condensed actin, which may compromise TJs function and BBB integrity (Park et al, 2013;Young et al, 2014). Using the bEnd.3 endothelial cell model, we have previously shown that METH-exposure led to a dramatic loss of F-actin integrity concomitant with claudin-5 downregulation and redistribution (Fernandes et al, 2014). In endothelial cells, these changes at the cytoskeleton level may lead to loss of adhesion and/or relevant restructuring of the endothelium, thus contributing to METH neurotoxicity.…”
Section: Discussionmentioning
confidence: 91%
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“…Previous studies showed that METH impacts actin filaments, leading to actin depolymerization, altered cell shape and local accumulation of condensed actin, which may compromise TJs function and BBB integrity (Park et al, 2013;Young et al, 2014). Using the bEnd.3 endothelial cell model, we have previously shown that METH-exposure led to a dramatic loss of F-actin integrity concomitant with claudin-5 downregulation and redistribution (Fernandes et al, 2014). In endothelial cells, these changes at the cytoskeleton level may lead to loss of adhesion and/or relevant restructuring of the endothelium, thus contributing to METH neurotoxicity.…”
Section: Discussionmentioning
confidence: 91%
“…Despite the previously reported protective properties of ALC (Pettegrew et al, 2000), its action at the cytoskeleton level is still poorly explored. We have recently shown that ALC effectively prevents METH-induced loss of alignment in endothelial actin filaments, through ILK mediated release of MMP-9 (Fernandes et al, 2014). Of note, ILK was also shown to mediate MMP-9-release through regulation of glycogen synthase (GSK)-3b activity (for review see McDonald et al, 2008), while GSK3b is known to interact and colocalize with HDAC6, enhancing its activity (Li et al, 2013).…”
Section: Discussionmentioning
confidence: 99%
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