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T-2 toxin-induced apoptosis involving Fas, p53, Bcl-xL, Bcl-2, Bax and caspase-3 signaling pathways in human chondrocytes / 浙江大学学报(英文版)(B辑:生物医学和生物技术)
Article in English | WPRIM (Western Pacific) | ID: wpr-359406
Responsible library: WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effects of T-2 toxin on expressions of Fas, p53, Bcl-xL, Bcl-2, Bax and caspase-3 on human chondrocytes.</p><p><b>METHODS</b>Human chondrocytes were treated with T-2 toxin (1-20 ng/ml) for 5 d. Fas, p53 and other apoptosis-related proteins such as Bax, Bcl-2, Bcl-xL, caspase-3 were determined by Western blot analysis and their mRNA expressions were determined by reverse transcriptase-polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>Increases in Fas, p53 and the pro-apoptotic factor Bax protein and mRNA expressions and a decrease of the anti-apoptotic factor Bcl-xL were observed in a dose-dependent manner after exposures to 1-20 ng/ml T-2 toxin, while the expression of the anti-apoptotic factor Bcl-2 was unchanged. Meanwhile, T-2 toxin could also up-regulate the expressions of both pro-caspase-3 and caspase-3 in a dose-dependent manner.</p><p><b>CONCLUSION</b>These data suggest a possible underlying molecular mechanism for T-2 toxin to induce the apoptosis signaling pathway in human chondrocytes by regulation of apoptosis-related proteins.</p>
Subject(s)
Full text: Available Database: WPRIM (Western Pacific) Main subject: T-2 Toxin / RNA, Messenger / Base Sequence / Signal Transduction / Gene Expression / Cells, Cultured / Blotting, Western / Tumor Suppressor Protein p53 / Apoptosis / DNA Primers Limits: Humans Language: English Journal: Journal of Zhejiang University. Science. B Year: 2008 Document type: Article
Full text: Available Database: WPRIM (Western Pacific) Main subject: T-2 Toxin / RNA, Messenger / Base Sequence / Signal Transduction / Gene Expression / Cells, Cultured / Blotting, Western / Tumor Suppressor Protein p53 / Apoptosis / DNA Primers Limits: Humans Language: English Journal: Journal of Zhejiang University. Science. B Year: 2008 Document type: Article
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