Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2009-8-4
pubmed:abstractText
Autophagic cell death has recently received a great deal of attention. However, a dependence of this type of cell death on the actual process of autophagy has only rarely been proven. Indeed, it is important to differentiate between cell death with an accumulation of autophagosomes and cell death actually caused by excessive or inhibited autophagy. The aim of this study was to elucidate the mechanism of action involved in the cytotoxicity of 1-O-hexadecyl-2-O-methyl-3-O-(2'-acetamido-2'-deoxy-beta-D-glucopyranosyl)-sn-glycerol (Gln) and specifically the involvement of autophagy in the effects observed. Our results show that Gln induces cell death associated with large increases in autophagolysosome number and size. However the cell death is independent of autophagy and caspase activation. Instead, Gln leads to lysosomal membrane permeabilization with a resulting leakage of hydrolases into the cytosol, which are then directly involved in cell death. The increased number of autophagolysosomes, however, is just a side effect of the neutralization of the lysosomal pH by Gln.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1554-8635
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
835-46
pubmed:dateRevised
2010-4-1
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
1-O-Hexadecyl-2-O-methyl-3-O-(2'-acetamido-2'-deoxy-beta-D-glucopyranosyl)-sn-glycerol (Gln) induces cell death with more autophagosomes which is autophagy-independent.
pubmed:affiliation
Department of Medical Genetics, Cambridge Institute for Medical Research, University of Cambridge, Cambridge, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't