2,3,7,8-tetrachlorodibenzo-p-dioxin regulates Bovine Herpesvirus type 1 induced apoptosis by modulating Bcl-2 family members
2,3,7,8-tetrachlorodibenzo-p-dioxin regulates Bovine Herpesvirus type 1 induced apoptosis by modulating Bcl-2 family members
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DOI：
10.1007/s10495-008-0249-y
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发表时间：
2008-10-01
期刊：
影响因子：
7.2
通讯作者：
Pagnini, Ugo
中科院分区：
文献类型：
--
作者：
Fiorito, Filomena;Marfe, Gabriella;Pagnini, Ugo
暴露于环境污染物，如2，3，7，8-四氯二苯并-对-二恶英（TCDD），导致对传染性病原体的易感性增加。用牛疱疹病毒1型（BHV-1）感染牛细胞（MDBK）预期病毒诱导的细胞凋亡，表明TCDD参与病毒感染。本文分析了TCDD对BHV-1感染MDBK细胞凋亡途径的影响。感染12小时后，TCDD诱导凋亡细胞的显着增加。与未暴露组相比，TCDD导致半胱天冬酶3、8和9的剂量依赖性上调和预期激活。与对照相比，TCDD预期PARP裂解。TCDD还能增加Bax和Bid的表达，降低Bcl-2和Bcl-XL的表达。这些事件在暴露的细胞中比未暴露的细胞更早发生。提示TCDD通过影响Bcl-2家族成员的表达和上调caspase的活性来影响BHV-1诱导的细胞凋亡。
Exposure to environmental contaminants, like 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), leads to an increased susceptibility to infectious agents. Infection of bovine cells (MDBK) with Bovine Herpesvirus 1 (BHV-1) anticipates virus-induced apoptosis, suggesting an involvement of TCDD in virus infection. Herein we analyzed the effects of TCDD on apoptotic pathway in MDBK cells infected with BHV-1. After 12 h of infection, TCDD induced a significant increase in apoptotic cells. TCDD caused a dose-dependent up-regulation and anticipated activation of caspases 3, 8 and 9, with respect to unexposed groups. TCDD anticipated cleavage of PARP, compared to controls. Furthermore TCDD increased Bax and Bid levels, and decreased Bcl-2 and Bcl-XL levels. Such events took place earlier in exposed than unexposed cells. These results showed that TCDD influences BHV-1 induced apoptosis through members of Bcl-2 family and up-regulating activation of caspases.