Linked Life Data

12858047

Source:http://linkedlifedata.com/resource/pubmed/id/12858047

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2003-7-14
pubmed:abstractText
Transforming growth factor (TGF)-beta1 is a key regulator of brain response to injury and inflammation. It exerts anti-inflammatory roles by inhibiting microglial proliferation and free radical induction. TGF-beta1 is known to induce apoptotic cell death of microglia in a Bcl-2-independent pathway. The purpose of this study was to examine detailed mechanisms of TGF-beta1-induced microglial apoptosis. Assays for cell viability and DNA fragmentation demonstrated that TGF-beta1 induced apoptotic cell death in primary rat microglial cultures. Reverse transcription (RT)-PCR analysis showed that primary microglial cells expressed mRNAs for rat inhibitor-of-apoptosis protein (RIAP)-1 and RIAP-3 under normal culture conditions and that treatment with TGF-beta1 resulted in a significant reduction in the amounts of RIAP-1 and RIAP-3 mRNAs. Because IAPs are potent suppressor of apoptotic cell death, decrease in IAP expression might provide an important regulatory function in TGF-beta1-mediated microglial death and in attenuation of excessive microglial activation in pathological conditions.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0959-4965
pubmed:author
pubmed:issnType
Print
pubmed:day
6
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
857-60
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Down-regulation of the expression of rat inhibitor-of-apoptosis protein-1 and -3 during transforming growth factor-beta1-mediated apoptosis in rat brain microglia.
pubmed:affiliation
Graduate School of East-West Medical Science, Kyung Hee University, Yong-In 499-701, Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't