Linked Life Data

17320289

Source:http://linkedlifedata.com/resource/pubmed/id/17320289

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-3-26
pubmed:abstractText
Neuronal apoptosis is crucial for central nervous system development and also contributes to neurodegenerative disease. Apolipoprotein-E (apoE) regulates brain lipid transport and specific neuronal functions and previous research, investigating non-neuronal cell types, identified an association between apoptosis and increased apoE expression. In the present study we used the human SK-N-SH neuronal cell line to investigate potential changes in apoE expression during apoptosis which occurs as a consequence of extended culture (up to 5 days) without replenishing trophic factors. Standard and real-time PCR analysis indicated a significant 6-fold increase in apoE mRNA after 3 days which was correlated with caspase-3 activation, TUNEL positivity and the formation of apoptotic bodies. ApoE protein levels were low in the absence of apoptosis but increased by 8-fold when apoptosis was induced. Analysis of cellular debris that accumulated in the culture supernatants indicated that apoE levels became progressively concentrated in apoptotic bodies. These data indicate that apoE is up-regulated during neuronal apoptosis and raise the possibility that apoE may play a role in the clearance of apoptotic bodies through apoE-receptor interactions.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0304-3940
pubmed:author
pubmed:issnType
Print
pubmed:day
12
pubmed:volume
416
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
206-10
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Apoptosis induces neuronal apolipoprotein-E synthesis and localization in apoptotic bodies.
pubmed:affiliation
Prince of Wales Medical Research Institute, Randwick, NSW 2031, Australia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't