KLF6 和 iNOS 调节呼吸道合胞病毒感染期间的细胞凋亡。
KLF6 and iNOS regulates apoptosis during respiratory syncytial virus infection.
机构信息
Department of Microbiology and Immunology, The University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, United States.
出版信息
Cell Immunol. 2013 May-Jun;283(1-2):1-7. doi: 10.1016/j.cellimm.2013.06.002. Epub 2013 Jun 18.
Abstract
Human respiratory syncytial virus (RSV) is a highly pathogenic lung-tropic virus that causes severe respiratory diseases. Enzymatic activity of inducible nitric oxide (iNOS) is required for NO generation. Although NO contributes to exaggerated lung disease during RSV infection, the role of NO in apoptosis during infection is not known. In addition, host trans-activator(s) required for iNOS gene expression during RSV infection is unknown. In the current study we have uncovered the mechanism of iNOS gene induction by identifying kruppel-like factor 6 (KLF6) as a critical transcription factor required for iNOS gene expression during RSV infection. Furthermore, we have also uncovered the role of iNOS as a critical host factor regulating apoptosis during RSV infection.
摘要
人类呼吸道合胞病毒（RSV）是一种高致病性的肺嗜性病毒，可引起严重的呼吸道疾病。诱导型一氧化氮合酶（iNOS）的酶活性是产生 NO 的必需条件。尽管 NO 在 RSV 感染期间导致肺部疾病加重，但 NO 在感染期间对细胞凋亡的作用尚不清楚。此外，RSV 感染时用于 iNOS 基因表达的宿主反式激活因子（trans-activator）也不清楚。在本研究中，我们通过鉴定 Kruppel 样因子 6（KLF6）作为 RSV 感染期间 iNOS 基因表达所必需的关键转录因子，揭示了 iNOS 基因诱导的机制。此外，我们还揭示了 iNOS 作为 RSV 感染期间调节细胞凋亡的关键宿主因子的作用。
相似文献
1
KLF6 and iNOS regulates apoptosis during respiratory syncytial virus infection.KLF6 和 iNOS 调节呼吸道合胞病毒感染期间的细胞凋亡。
Cell Immunol. 2013 May-Jun;283(1-2):1-7. doi: 10.1016/j.cellimm.2013.06.002. Epub 2013 Jun 18.
2
Transactivation of inducible nitric oxide synthase gene by Kruppel-like factor 6 regulates apoptosis during influenza A virus infection.Kruppel 样因子 6 诱导诱导型一氧化氮合酶基因的转录激活调控甲型流感病毒感染期间的细胞凋亡。
J Immunol. 2012 Jul 15;189(2):606-15. doi: 10.4049/jimmunol.1102742. Epub 2012 Jun 18.
3
Krüppel-like factor 6 regulates transforming growth factor-β gene expression during human respiratory syncytial virus infection.Krüppel 样因子 6 在人类呼吸道合胞病毒感染期间调节转化生长因子-β 基因表达。
Virol J. 2011 Aug 17;8:409. doi: 10.1186/1743-422X-8-409.
4
Human respiratory syncytial virus non-structural protein NS1 modifies miR-24 expression via transforming growth factor-β.人呼吸道合胞病毒非结构蛋白NS1通过转化生长因子-β调节miR-24的表达。
J Gen Virol. 2015 Nov;96(11):3179-3191. doi: 10.1099/jgv.0.000261.
5
Respiratory syncytial virus inhibits lung epithelial Na+ channels by up-regulating inducible nitric-oxide synthase.呼吸道合胞病毒通过上调诱导型一氧化氮合酶来抑制肺上皮钠通道。
J Biol Chem. 2009 Mar 13;284(11):7294-306. doi: 10.1074/jbc.M806816200. Epub 2009 Jan 8.
6
Transcriptional activation of the human inducible nitric-oxide synthase promoter by Kruppel-like factor 6.Kruppel样因子6对人诱导型一氧化氮合酶启动子的转录激活作用。
J Biol Chem. 2003 Apr 25;278(17):14812-9. doi: 10.1074/jbc.M300787200. Epub 2003 Feb 16.
7
8
Immune and functional role of nitric oxide in a mouse model of respiratory syncytial virus infection.一氧化氮在呼吸道合胞病毒感染小鼠模型中的免疫及功能作用
J Infect Dis. 2005 Feb 1;191(3):387-95. doi: 10.1086/427241. Epub 2004 Dec 22.
9
Nitric oxide production is downregulated during respiratory syncytial virus persistence by constitutive expression of arginase 1.一氧化氮的产生在呼吸道合胞病毒持续感染期间被下调，这是由精氨酸酶 1 的组成性表达引起的。
Arch Virol. 2019 Sep;164(9):2231-2241. doi: 10.1007/s00705-019-04259-0. Epub 2019 Jun 8.
10
Krüppel-like factor 4, a novel transcription factor regulates microglial activation and subsequent neuroinflammation.Krüppel 样因子 4，一种新型转录因子，调节小胶质细胞的激活和随后的神经炎症。
J Neuroinflammation. 2010 Oct 15;7:68. doi: 10.1186/1742-2094-7-68.
引用本文的文献
1
Myeloid Cell Leukemia-1 knockout leads to increased viral propagation of Respiratory Syncytial Virus and influenza virus in mouse embryonic fibroblast cells and A549 cells: implications in cancer therapy.髓样细胞白血病-1基因敲除导致呼吸道合胞病毒和流感病毒在小鼠胚胎成纤维细胞和A549细胞中的病毒增殖增加：对癌症治疗的启示。
Front Cell Infect Microbiol. 2025 Aug 29;15:1615790. doi: 10.3389/fcimb.2025.1615790. eCollection 2025.
2
Silencing KLF6 Alleviates Cigarette Smoke Extract-Induced Mitochondrial Dysfunction in Bronchial Epithelial Cells by SIRT4 Upregulation.沉默 KLF6 通过上调 SIRT4 缓解香烟烟雾提取物诱导的支气管上皮细胞线粒体功能障碍。
Int J Chron Obstruct Pulmon Dis. 2024 Mar 23;19:815-828. doi: 10.2147/COPD.S451264. eCollection 2024.
3
Human beta defensin-3 mediated activation of β-catenin during human respiratory syncytial virus infection: interaction of HBD3 with LDL receptor-related protein 5.人呼吸道合胞病毒感染期间人β-防御素-3介导的β-连环蛋白激活：HBD3与低密度脂蛋白受体相关蛋白5的相互作用
Front Microbiol. 2023 Jun 22;14:1186510. doi: 10.3389/fmicb.2023.1186510. eCollection 2023.
4
KLF6 facilitates differentiation of odontoblasts through modulating the expression of P21 in vitro.KLF6 通过调节 P21 的表达促进体外成牙本质细胞的分化。
Int J Oral Sci. 2022 Apr 14;14(1):20. doi: 10.1038/s41368-022-00172-6.
5
Oxidative Stress-Related Mechanisms in SARS-CoV-2 Infections.氧化应激相关机制在 SARS-CoV-2 感染中的作用。
Oxid Med Cell Longev. 2022 Mar 8;2022:5589089. doi: 10.1155/2022/5589089. eCollection 2022.
6
Can FeNO be a biomarker in the post-COVID-19 patients monitoring?新冠病毒感染后患者的监测中呼出气一氧化氮（FeNO）能否作为生物标志物？
Respir Med. 2022 Mar;193:106745. doi: 10.1016/j.rmed.2022.106745. Epub 2022 Jan 26.
7
Two Sides of the Same Coin: The Roles of KLF6 in Physiology and Pathophysiology.两面一体：KLF6 在生理学和病理生理学中的作用。
Biomolecules. 2020 Sep 28;10(10):1378. doi: 10.3390/biom10101378.
8
Alveolar Macrophages Treated With Spore Protect Mice Infected With Respiratory Syncytial Virus A2.用孢子处理的肺泡巨噬细胞可保护感染呼吸道合胞病毒A2的小鼠。
Front Microbiol. 2019 Mar 12;10:447. doi: 10.3389/fmicb.2019.00447. eCollection 2019.
9
Prediction of key genes and miRNAs responsible for loss of muscle force in patients during an acute exacerbation of chronic obstructive pulmonary disease.慢性阻塞性肺疾病急性加重期患者肌肉力量丧失相关关键基因和微小RNA的预测
Int J Mol Med. 2016 Nov;38(5):1450-1462. doi: 10.3892/ijmm.2016.2761. Epub 2016 Sep 30.
10
The innate immune response to RSV: Advances in our understanding of critical viral and host factors.对呼吸道合胞病毒的先天性免疫反应：我们对关键病毒和宿主因素理解的进展
Vaccine. 2017 Jan 11;35(3):481-488. doi: 10.1016/j.vaccine.2016.09.030. Epub 2016 Sep 28.
本文引用的文献
1
Transactivation of inducible nitric oxide synthase gene by Kruppel-like factor 6 regulates apoptosis during influenza A virus infection.Kruppel 样因子 6 诱导诱导型一氧化氮合酶基因的转录激活调控甲型流感病毒感染期间的细胞凋亡。
J Immunol. 2012 Jul 15;189(2):606-15. doi: 10.4049/jimmunol.1102742. Epub 2012 Jun 18.
2
Krüppel-like factor 6 regulates transforming growth factor-β gene expression during human respiratory syncytial virus infection.Krüppel 样因子 6 在人类呼吸道合胞病毒感染期间调节转化生长因子-β 基因表达。
Virol J. 2011 Aug 17;8:409. doi: 10.1186/1743-422X-8-409.
3
TGF-β2 reduces nitric oxide synthase mRNA through a ROCK-dependent pathway in airway epithelial cells.TGF-β2 通过 ROCK 依赖性途径减少气道上皮细胞中的一氧化氮合酶 mRNA。
Am J Physiol Lung Cell Mol Physiol. 2011 Sep;301(3):L361-7. doi: 10.1152/ajplung.00464.2010. Epub 2011 Jun 17.
4
Viral pneumonia.病毒性肺炎。
Lancet. 2011 Apr 9;377(9773):1264-75. doi: 10.1016/S0140-6736(10)61459-6. Epub 2011 Mar 22.
5
Increased inducible nitric oxide synthase expression in organs is associated with a higher severity of H5N1 influenza virus infection.器官中诱导型一氧化氮合酶表达的增加与 H5N1 流感病毒感染的严重程度更高有关。
PLoS One. 2011 Jan 19;6(1):e14561. doi: 10.1371/journal.pone.0014561.
6
The airway epithelium: soldier in the fight against respiratory viruses.气道上皮：抗击呼吸道病毒的战士。
Clin Microbiol Rev. 2011 Jan;24(1):210-29. doi: 10.1128/CMR.00014-10.
7
Mammalian Krüppel-like factors in health and diseases.哺乳动物 Krüppel 样因子在健康和疾病中的作用。
Physiol Rev. 2010 Oct;90(4):1337-81. doi: 10.1152/physrev.00058.2009.
8
Exhaled nitric oxide in acute respiratory syncytial virus bronchiolitis.急性呼吸道合胞病毒细支气管炎中的呼出一氧化氮
Arch Pediatr Adolesc Med. 2010 Aug;164(8):727-31. doi: 10.1001/archpediatrics.2010.128.
9
Regulation of the expression of inducible nitric oxide synthase.诱导型一氧化氮合酶表达的调控。
Nitric Oxide. 2010 Sep 15;23(2):75-93. doi: 10.1016/j.niox.2010.04.007. Epub 2010 May 8.
10
Highly pathogenic avian influenza A virus H5N1 NS1 protein induces caspase-dependent apoptosis in human alveolar basal epithelial cells.高致病性禽流感病毒 H5N1 NS1 蛋白诱导人肺泡基底上皮细胞中的 caspase 依赖性细胞凋亡。
Virol J. 2010 Mar 3;7:51. doi: 10.1186/1743-422X-7-51.
Zotero 插件