About: Methamphetamine induces autophagy as a pro-survival response against apoptotic endothelial cell death through the Kappa opioid receptor

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About: Methamphetamine induces autophagy as a pro-survival response against apoptotic endothelial cell death through the Kappa opioid receptor Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Methamphetamine induces autophagy as a pro-survival response against apoptotic endothelial cell death through the Kappa opioid receptor
Creator	Banerjee, S Ma, J Meng, J Ramakrishnan, S Roy, S Wan, J
Source	Medline; PMC
abstract	Methamphetamine (METH) is a psychostimulant with high abuse potential and severe neurotoxicity. Recent studies in animal models have indicated that METH can impair the blood–brain barrier (BBB), suggesting that some of the neurotoxic effects resulting from METH abuse could be due to barrier disruption. We report here that while chronic exposure to METH disrupts barrier function of primary human brain microvascular endothelial cells (HBMECs) and human umbilical vein endothelial cells (HUVECs), an early pro-survival response is observed following acute exposure by induction of autophagic mechanisms. Acute METH exposure induces an early increase in Beclin1 and LC3 recruitment. This is mediated through inactivation of the protein kinase B (Akt)/mammalian target of rapamycin (mTOR)/p70S6K pathway, and upregulation of the ERK1/2. Blockade of Kappa opioid receptor (KOR), and treatment with autophagic inhibitors accelerated METH-induced apoptosis, suggesting that the early autophagic response is a survival mechanism for endothelial cells and is mediated through the kappa opioid receptor. Our studies indicate that kappa opioid receptor can be therapeutically exploited for attenuating METH-induced BBB dysfunction.
has issue date	2014-03-06(xsd:dateTime)
bibo:doi	10.1038/cddis.2014.64
bibo:pmid	24603327
has license	cc-by-nc-nd
sha1sum (hex)	2159d7f128a1995e7131a8d4f036fcb3cec6e332
schema:url	https://doi.org/10.1038/cddis.2014.64
resource representing a document's title	Methamphetamine induces autophagy as a pro-survival response against apoptotic endothelial cell death through the Kappa opioid receptor
has PubMed Central identifier	PMC3973232
has PubMed identifier	24603327
schema:publication	Cell Death Dis
resource representing a document's body	covid:2159d7f128a1995e7131a8d4f036fcb3cec6e332#body_text
is schema:about of	named entity 'target' named entity 'mechanisms' named entity 'accelerated' named entity 'upregulation' named entity 'human brain' named entity 'response' named entity 'Methamphetamine' named entity 'opioid receptor' named entity 'studies' named entity 'high' named entity 'endothelial cell' named entity 'Methamphetamine' named entity 'induces' named entity 'apoptotic' covid:arg/2159d7f128a1995e7131a8d4f036fcb3cec6e332 named entity 'neurotoxicity' named entity 'mediated' named entity 'Recent' named entity 'mTOR' named entity 'autophagic' named entity 'LC3' named entity 'effects' named entity 'apoptosis' named entity 'autophagy' named entity 'abuse potential' named entity 'BBB' named entity 'protein kinase' named entity 'autophagic' named entity 'neurotoxicity' named entity 'human brain' named entity 'mTOR' named entity 'endothelial cells' named entity 'METH' named entity 'METH' named entity 'Methamphetamine' named entity 'psychostimulant' named entity 'METH' named entity 'apoptotic' named entity 'endothelial cell' named entity 'Beclin1' named entity 'Beclin1' named entity 'METH' named entity 'brain microvascular' named entity 'METH' named entity 'Apoptosis' named entity 'antagonist' named entity 'pathological conditions' named entity 'dopaminergic' named entity 'endothelial cells' named entity 'excitotoxicity' named entity 'vacuoles' named entity 'amphetamine' named entity 'glycosylated' named entity 'BBB' named entity 'caspase-3' named entity 'mitogen-activated protein kinase 1' named entity 'METH' named entity 'ultramicrotome' named entity 'protein' named entity 'Methamphetamine' named entity 'Lysosomal degradation' named entity 'siRNA' named entity 'pepstatin' named entity 'osmium tetroxide' named entity 'Beclin1' named entity 'autophagy' named entity 'autophagy' named entity 'Autophagy' named entity 'transfection' named entity 'METH' named entity 'LC3' named entity 'Apoptosis' named entity 'METH' named entity 'autophagy' named entity 'apoptosis' named entity 'Life Technologies'

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