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pubmed-article:12858047pubmed:abstractTextTransforming 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.lld:pubmed
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pubmed-article:12858047pubmed:articleTitleDown-regulation of the expression of rat inhibitor-of-apoptosis protein-1 and -3 during transforming growth factor-beta1-mediated apoptosis in rat brain microglia.lld:pubmed
pubmed-article:12858047pubmed:affiliationGraduate School of East-West Medical Science, Kyung Hee University, Yong-In 499-701, Korea.lld:pubmed
pubmed-article:12858047pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:12858047pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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