Linked Life Data

15953367

Source:http://linkedlifedata.com/resource/pubmed/id/15953367

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-6-14
pubmed:abstractText
Brain microglial cells are thought to undergo apoptosis following the exposure to inflammatory stimuli such as lipopolysaccharide (LPS) and IFNgamma, which is considered as an autoregulatory mechanism to control their own activation state. Here, we report that N-myc constitutes a novel apoptotic pathway of LPS/IFNgamma-activated microglia. The expression of N-myc was synergistically enhanced by LPS and IFNgamma in microglia. Tetracycline-based conditional expression of N-myc sensitized microglia to nitric oxide (NO)-induced apoptosis. Knockdown of N-myc expression using small interfering RNA (siRNA) attenuated LPS/IFNgamma-induced microglial apoptosis. An increase in N-myc expression, however, did not affect microglial production of NO or TNFalpha. The synergistic effect of LPS/IFNgamma on the microglial N-myc induction was mediated through Janus kinase (JAK)/STAT1 (signal transducer and activator of transcription 1) pathway. Taken together, LPS/IFNgamma-induced N-myc participated in the activation-induced cell death of microglia by sensitizing the cells to NO-induced apoptosis; however, N-myc did not influence the processes of inflammatory activation of microglia.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-3042
pubmed:author
pubmed:issnType
Print
pubmed:volume
94
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
249-56
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Pro-apoptotic activity of N-myc in activation-induced cell death of microglia.
pubmed:affiliation
Department of Pharmacology, Kyungpook National University School of Medicine, Daegu, Korea.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't