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短裸甲藻毒素 2 改变 Jurkat 细胞中凋亡、DNA 损伤和细胞因子基因的表达。

Brevetoxin 2 alters expression of apoptotic, DNA damage, and cytokine genes in Jurkat cells.

机构信息

Department of Environmental and Molecular Toxicology, North Carolina State University, Raleigh, North Carolina, USA.

出版信息

Hum Exp Toxicol. 2011 Mar;30(3):182-91. doi: 10.1177/0960327110372644. Epub 2010 May 24.

DOI:10.1177/0960327110372644
PMID:20498034
Abstract

Brevetoxins are potent neurotoxins that exert their toxicity through activation of voltage-gated sodium channels. Exposure to brevetoxins cause severe respiratory inflammation in marine mammals and humans. Brevetoxin activation of voltage-gated sodium channels on immune cells can lead to several biological responses including cell proliferation, gene transcription, cytokine production and even apoptosis. Jurkat E6-1 T cells were treated with brevetoxin 2 for 4 hours at a dose previously shown to induce apoptosis and DNA damage. Changes in gene expression were then assessed via PCR arrays. Gene expression analysis revealed significant change in expression of 17 genes related to apoptosis, 21 genes related to DNA damage signaling, and 19 genes encoding common cytokines. The gene expression data supports the idea that brevetoxins trigger complex reactions involving both inflammation and cell death.

摘要

短裸甲藻毒素是一种强效的神经毒素,通过激活电压门控钠离子通道发挥其毒性。暴露于短裸甲藻毒素会导致海洋哺乳动物和人类发生严重的呼吸道炎症。短裸甲藻毒素激活免疫细胞上的电压门控钠离子通道可导致多种生物学反应,包括细胞增殖、基因转录、细胞因子产生,甚至细胞凋亡。先前的研究已表明,用 Brevetoxin 2 处理 Jurkat E6-1 T 细胞 4 小时可诱导细胞凋亡和 DNA 损伤。然后通过 PCR 阵列评估基因表达变化。基因表达分析显示,与细胞凋亡相关的 17 个基因、与 DNA 损伤信号相关的 21 个基因和编码常见细胞因子的 19 个基因的表达发生了显著变化。基因表达数据支持短裸甲藻毒素触发涉及炎症和细胞死亡的复杂反应的观点。

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