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学科主题临床医学
NF-kappaB mediates the survival of human bronchial epithelial cells exposed to cigarette smoke extract
Liu, Xiangde1; Togo, Shinsaku2; Al-Mugotir, Mona1; Kim, Huijung3; Fang, QiuHong4; Kobayashi, Tetsu5; Wang, XingQi1; Mao, Lijun6; Bitterman, Peter7; Rennard, Stephen1
刊名RESPIRATORY RESEARCH
2008-09-23
DOI10.1186/1465-9921-9-66
9
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Respiratory System
资助者American Lung Association (XL) ; Larson Endowment ; University of Nebraska Medical Center (SIR) ; American Lung Association (XL) ; Larson Endowment ; University of Nebraska Medical Center (SIR)
研究领域[WOS]Respiratory System
关键词[WOS]PROSTATE-CANCER CELLS ; DNA-DAMAGE ; CARCINOMA-CELLS ; B ACTIVATION ; APOPTOSIS ; CURCUMIN ; STAT3 ; TRANSCRIPTION ; INHIBITION ; EXPRESSION
英文摘要

Background: We have previously reported that low concentrations of cigarette smoke extract induce DNA damage without leading to apoptosis or necrosis in human bronchial epithelial cells (HBECs), and that IL-6/STAT3 signaling contributes to the cell survival. Since NF-kappa B is also involved in regulating apoptosis and cell survival, the current study was designed to investigate the role of NF-kappa B in mediating cell survival in response to cigarette smoke exposure in HBECs.

Methods: Both the pharmacologic inhibitor of NF-kappa B, curcumin, and RNA interference targeting p65 were used to block NF-kappa B signaling in HBECs. Apoptosis and cell survival were then assessed by various methods including COMET assay, LIVE/DEAD Cytotoxicity/Viability assay and colony formation assay.

Results: Cigarette smoke extract (CSE) caused DNA damage and cell cycle arrest in S phase without leading to apoptosis in HBECs as evidenced by TUNEL assay, COMET assay and DNA content assay. CSE stimulated NF-kappa B -DNA binding activity and up-regulated Bcl-XL protein in HBECs. Inhibition of NF-kappa B by the pharmacologic inhibitor curcumin (20 mu M) or suppression of p65 by siRNA resulted in a significant increase in cell death in response to cigarette smoke exposure. Furthermore, cells lacking p65 were incapable of forming cellular colonies when these cells were exposed to CSE, while they behaved normally in the regular culture medium.

Conclusion: The current study demonstrates that CSE activates NF-kappa B and up-regulates Bcl-XL through NF-kappa B activation in HBECs, and that CSE induces cell death in cells lacking p65. These results suggest that activation of NF-kappa B regulates cell survival following DNA damage by cigarette smoke in human bronchial epithelial cells.

语种英语
资助者American Lung Association (XL) ; Larson Endowment ; University of Nebraska Medical Center (SIR) ; American Lung Association (XL) ; Larson Endowment ; University of Nebraska Medical Center (SIR)
WOS记录号WOS:000260432600001
引用统计
被引频次:38[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/56688
专题北京大学第三临床医学院
作者单位1.Juntendo Univ, Sch Med, Tokyo 113, Japan
2.Won Kwang Univ, Kunpo Med Ctr, Seoul, South Korea
3.Mie Univ, Grad Sch Med, Tsu, Mie 514, Japan
4.Peking Univ, Hosp 3, Beijing 100871, Peoples R China
5.Univ Minnesota, Minneapolis, MN USA
6.Univ Nebraska Med Ctr, Dept Internal Med, Omaha, NE USA
7.Peking Univ, Beijing Shijitan Hosp, Beijing 100871, Peoples R China
推荐引用方式
GB/T 7714
Liu, Xiangde,Togo, Shinsaku,Al-Mugotir, Mona,et al. NF-kappaB mediates the survival of human bronchial epithelial cells exposed to cigarette smoke extract[J]. RESPIRATORY RESEARCH,2008,9.
APA Liu, Xiangde.,Togo, Shinsaku.,Al-Mugotir, Mona.,Kim, Huijung.,Fang, QiuHong.,...&Rennard, Stephen.(2008).NF-kappaB mediates the survival of human bronchial epithelial cells exposed to cigarette smoke extract.RESPIRATORY RESEARCH,9.
MLA Liu, Xiangde,et al."NF-kappaB mediates the survival of human bronchial epithelial cells exposed to cigarette smoke extract".RESPIRATORY RESEARCH 9(2008).
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