Comparative proteomic analysis reveals heart toxicity induced by chronic arsenic exposure in rats
Comparative proteomic analysis reveals heart toxicity induced by chronic arsenic exposure in rats
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比较蛋白质组学分析揭示了大鼠慢性砷暴露引起的心脏毒性
DOI：
10.1016/j.envpol.2017.05.077
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发表时间：
2017
影响因子：
8.9
通讯作者：
Shen Heqing
中科院分区：
文献类型：
--
作者：
Huang Qingyu;Xi Guochen;Alamdar Ambreen;Zhang Jie;Shen Heqing
砷是一种广泛存在于环境中的类金属，对人体健康有着广泛的危害。然而，砷引起的心脏毒性的全球观点仍然缺乏，潜在的分子机制仍然不清楚。本研究旨在通过比较定量蛋白质组学分析，研究长期砷暴露后大鼠心脏蛋白质组的变化。结果，我们发现81种蛋白质的丰度被砷处理显著改变（35种上调，46种下调）。其中，33种蛋白质与心血管系统发育和功能特异性相关，包括心脏发育、心脏形态、心脏收缩和扩张以及其他心血管功能。砷对14种蛋白质的异常调节可能通过Akt/p38 MAPK信号通路介导，干扰大鼠心脏的收缩和舒张功能，损害心脏的形态发生和发育，并诱导血栓形成。总的来说，这些发现将增加我们对相关机制的了解，并为环境砷暴露诱导的心脏毒性开发有用的生物标志物。
Arsenic is a widespread metalloid in the environment, which poses a broad spectrum of adverse effects on human health. However, a global view of arsenic-induced heart toxicity is still lacking, and the underlying molecular mechanisms remain unclear. By performing a comparative quantitative proteomic analysis, the present study aims to investigate the alterations of proteome profile in rat heart after long-term exposure to arsenic. As a result, we found that the abundance of 81 proteins were significantly altered by arsenic treatment (35 up-regulated and 46 down-regulated). Among these, 33 proteins were specifically associated with cardiovascular system development and function, including heart development, heart morphology, cardiac contraction and dilation, and other cardiovascular functions. It is further proposed that the aberrant regulation of 14 proteins induced by arsenic would disturb cardiac contraction and relaxation, impair heart morphogenesis and development, and induce thrombosis in rats, which is mediated by the Akt/p38 MAPK signaling pathway. Overall, these findings will augment our knowledge of the involved mechanisms and develop useful biomarkers for cardiotoxicity induced by environmental arsenic exposure.