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本文引用的文献

1
Fibroblast growth factor-10 prevents H2O2-induced cell cycle arrest by regulation of G1 cyclins and cyclin dependent kinases.成纤维细胞生长因子-10通过调节G1期细胞周期蛋白和细胞周期蛋白依赖性激酶来防止过氧化氢诱导的细胞周期停滞。
FEBS Lett. 2007 Jan 23;581(2):248-52. doi: 10.1016/j.febslet.2006.12.020. Epub 2006 Dec 18.
2
Lung surfactant gelation induced by epithelial cells exposed to air pollution or oxidative stress.暴露于空气污染或氧化应激的上皮细胞诱导肺表面活性物质凝胶化。
Am J Respir Cell Mol Biol. 2005 Aug;33(2):161-8. doi: 10.1165/rcmb.2004-0365OC. Epub 2005 Apr 28.
3
Particulate matter induces alveolar epithelial cell DNA damage and apoptosis: role of free radicals and the mitochondria.颗粒物诱导肺泡上皮细胞DNA损伤和凋亡：自由基和线粒体的作用
Am J Respir Cell Mol Biol. 2003 Aug;29(2):180-7. doi: 10.1165/rcmb.2002-0269OC. Epub 2003 Feb 21.
4
Cyclin A- and cyclin E-Cdk complexes shuttle between the nucleus and the cytoplasm.细胞周期蛋白A和细胞周期蛋白E-Cdk复合物在细胞核和细胞质之间穿梭。
Mol Biol Cell. 2002 Mar;13(3):1030-45. doi: 10.1091/mbc.01-07-0361.
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Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution.肺癌、心肺死亡率与长期暴露于细颗粒物空气污染
JAMA. 2002 Mar 6;287(9):1132-41. doi: 10.1001/jama.287.9.1132.
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Biologic effects of oil fly ash.油飞灰的生物学效应。
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7
H2O2 induces a transient multi-phase cell cycle arrest in mouse fibroblasts through modulating cyclin D and p21Cip1 expression.过氧化氢通过调节细胞周期蛋白D和p21Cip1的表达，在小鼠成纤维细胞中诱导短暂的多阶段细胞周期停滞。
J Biol Chem. 2002 Apr 19;277(16):13761-70. doi: 10.1074/jbc.M111123200. Epub 2002 Feb 4.
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Role of cyclins in epithelial response to oxidants.细胞周期蛋白在上皮细胞对氧化剂反应中的作用。
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9
The cyclin-dependent kinase inhibitor p21 protects the lung from oxidative stress.细胞周期蛋白依赖性激酶抑制剂p21可保护肺部免受氧化应激的影响。
Am J Respir Cell Mol Biol. 2001 Jun;24(6):703-10. doi: 10.1165/ajrcmb.24.6.4355.
10
Pathways governing G1/S transition and their response to DNA damage.调控G1/S期转换的信号通路及其对DNA损伤的反应。
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环境颗粒物诱导肺泡上皮细胞周期停滞：G1 期细胞周期蛋白的作用。

Ambient particulate matter induces alveolar epithelial cell cycle arrest: role of G1 cyclins.

作者信息

Zhang Jingmei, Ghio Andrew J, Gao Mingxing, Wei Ke, Rosen Glenn D, Upadhyay Daya

机构信息

Department of Pulmonary and Critical Care Medicine, Stanford University Medical Center, 300 Pasteur Drive, Stanford, CA 94305, USA.

出版信息

FEBS Lett. 2007 Nov 13;581(27):5315-20. doi: 10.1016/j.febslet.2007.10.020. Epub 2007 Oct 23.

DOI:10.1016/j.febslet.2007.10.020
PMID:17977533
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2140149/
Abstract

We hypothesized that the ambient air pollution particles (particulate matter; PM) induce cell cycle arrest in alveolar epithelial cells (AEC). Exposure of PM (25microg/cm(2)) to AEC induced cells cycle arrest in G1 phase, inhibited DNA synthesis, blocked cell proliferation and caused decrease in cyclin E, A, D1 and Cyclin E- cyclin-dependent kinase (CDK)-2 kinase activity after 4h. PM induced upregulation of CDK inhibitor, p21 protein and p21 activity in AEC. SiRNAp21 blocked PM-induced downregulation of cyclins and AEC G1 arrest. Accordingly, we provide the evidence that PM induces AEC G1 arrest by altered regulation of G1 cyclins and CDKs.

摘要

我们假设环境空气污染颗粒（颗粒物；PM）可诱导肺泡上皮细胞（AEC）的细胞周期停滞。将PM（25μg/cm²）暴露于AEC后，4小时内可诱导细胞周期停滞于G1期，抑制DNA合成，阻断细胞增殖，并导致细胞周期蛋白E、A、D1及细胞周期蛋白E-细胞周期蛋白依赖性激酶（CDK）-2激酶活性降低。PM可诱导AEC中CDK抑制剂、p21蛋白及p21活性上调。SiRNAp21可阻断PM诱导的细胞周期蛋白下调及AEC G1期停滞。因此，我们提供了证据表明PM通过改变G1期细胞周期蛋白和CDK的调节来诱导AEC G1期停滞。