The roles of inducible chromatin and transcriptional memory in cellular defense system responses to redox-active pollutants.
The roles of inducible chromatin and transcriptional memory in cellular defense system responses to redox-active pollutants.
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DOI：
10.1016/j.freeradbiomed.2021.03.018
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发表时间：
2021-07
影响因子：
7.4
通讯作者：
Weinhouse C
中科院分区：
文献类型：
--
作者：
Weinhouse C
人们暴露在各种具有氧化还原活性的环境污染物中。空气污染、重金属、杀虫剂和内分泌干扰物会破坏细胞的氧化还原状态。我们环境中的氧化还原活性污染物都会触发它们自己的一组特定的细胞反应，但它们也会激活一组常见的一般应激反应，以缓冲细胞免受动态平衡的伤害。这些细胞防御系统(CDS)途径包括热休克反应、氧化应激反应、低氧反应、未折叠蛋白反应、DNA损伤反应以及由应激激活的p38丝裂原活化蛋白激酶介导的一般应激反应。在过去的二十年里，环境表观遗传学领域研究了表观遗传学对环境污染物的反应，包括氧化还原活性污染物。对这些反应的研究突出了染色质修饰在控制对污染物的转录反应中的作用，以及转录记忆的作用，通常被称为“表观遗传重编程”，使先前暴露的个体在二次挑战时容易产生更强大的转录反应。我在这篇综述中的中心论点是，高剂量或长期暴露于氧化还原活性污染物会导致CDS靶基因的转录记忆，从而影响细胞启动保护性反应的能力。为了支持这篇论文，我将：(1)总结已知的可诱导基因激活所需的染色质特征；(2)综述已知的转录记忆形式；(3)讨论可诱导染色质和转录记忆在氧化还原活性环境污染物激活的CDS反应中的作用；(4)提出CDS途径响应的概念框架，作为细胞对氧化还原活性污染物暴露的读数。
People are exposed to wide range of redox-active environmental pollutants. Air pollution, heavy metals, pesticides, and endocrine disrupting chemicals can disrupt cellular redox status. Redox-active pollutants in our environment all trigger their own sets of specific cellular responses, but they also activate a common set of general stress responses that buffer the cell against homeostatic insults. These cellular defense system (CDS) pathways include the heat shock response, the oxidative stress response, the hypoxia response, the unfolded protein response, the DNA damage response, and the general stress response mediated by the stress-activated p38 mitogen-activated protein kinase. Over the past two decades, the field of environmental epigenetics has investigated epigenetic responses to environmental pollutants, including redox-active pollutants. Studies of these responses highlight the role of chromatin modifications in controlling the transcriptional response to pollutants and the role of transcriptional memory, often referred to as “epigenetic reprogramming”, in predisposing previously exposed individuals to more potent transcriptional responses on secondary challenge. My central thesis in this review is that high dose or chronic exposure to redox-active pollutants leads to transcriptional memories at CDS target genes that influence the cell’s ability to mount protective responses. To support this thesis, I will: (1) summarize the known chromatin features required for inducible gene activation; (2) review the known forms of transcriptional memory; (3) discuss the roles of inducible chromatin and transcriptional memory in CDS responses that are activated by redox-active environmental pollutants; and (4) propose a conceptual framework for CDS pathway responsiveness as a readout of total cellular exposure to redox-active pollutants.
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