T-2 toxin-induced apoptosis involving Fas, p53, Bcl-xL, Bcl-2, Bax and caspase-3 signaling pathways in human chondrocytes.
- Author:
Jing-hong CHEN
1
;
Jun-ling CAO
;
Yong-lie CHU
;
Zhi-lun WANG
;
Zhan-tian YANG
;
Hong-lin WANG
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; Base Sequence; Blotting, Western; Caspase 3; genetics; metabolism; Cell Proliferation; drug effects; Cells, Cultured; Chondrocytes; cytology; drug effects; metabolism; DNA Primers; genetics; Gene Expression; drug effects; Humans; Proto-Oncogene Proteins c-bcl-2; genetics; metabolism; RNA, Messenger; genetics; metabolism; Reverse Transcriptase Polymerase Chain Reaction; Signal Transduction; drug effects; T-2 Toxin; toxicity; Tumor Suppressor Protein p53; genetics; metabolism; bcl-2-Associated X Protein; genetics; metabolism; bcl-X Protein; genetics; metabolism; fas Receptor; genetics; metabolism
- From: Journal of Zhejiang University. Science. B 2008;9(6):455-463
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate the effects of T-2 toxin on expressions of Fas, p53, Bcl-xL, Bcl-2, Bax and caspase-3 on human chondrocytes.
METHODSHuman 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).
RESULTSIncreases 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.
CONCLUSIONThese 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.
