小窝蛋白-1启动子氧化应激反应元件的定位
Mapping of oxidative stress response elements of the caveolin-1 promoter.
作者信息
Bartholomew Janine N, Galbiati Ferruccio
机构信息
Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
出版信息
Methods Mol Biol. 2010;594:409-23. doi: 10.1007/978-1-60761-411-1_29.
Abstract
According to the "free radical theory" of aging, normal aging occurs as the result of tissue damages inflicted by reactive oxygen species (ROS). ROS are known to induce cellular senescence, and senescent cells are believed to contribute to organismal aging. The molecular mechanisms that mediate the cellular response to oxidants remain to be fully identified. We have shown that oxidative stress induces cellular senescence through activation of the caveolin-1 promoter and upregulation of caveolin-1 protein expression. Here, we describe how reactive oxygen species activate the caveolin-1 promoter and how the signaling may be assayed. These approaches provide insight into the functional role of caveolin-1 and potentially allow the identification of novel ROS-regulated genes that are part of the signaling machinery regulating cellular senescence/aging.
摘要
根据衰老的“自由基理论”，正常衰老乃是活性氧（ROS）造成组织损伤的结果。已知ROS可诱导细胞衰老，且衰老细胞被认为会导致机体衰老。介导细胞对氧化剂反应的分子机制仍有待充分明确。我们已经表明，氧化应激通过激活小窝蛋白-1启动子和上调小窝蛋白-1蛋白表达来诱导细胞衰老。在此，我们描述活性氧如何激活小窝蛋白-1启动子以及如何检测该信号传导。这些方法为深入了解小窝蛋白-1的功能作用提供了思路，并有可能识别出作为调节细胞衰老/老化信号机制一部分的新型ROS调控基因。
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Oxidative stress induces premature senescence by stimulating caveolin-1 gene transcription through p38 mitogen-activated protein kinase/Sp1-mediated activation of two GC-rich promoter elements.氧化应激通过p38丝裂原活化蛋白激酶/Sp1介导的两个富含GC的启动子元件激活来刺激小窝蛋白-1基因转录，从而诱导细胞早衰。
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