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学科主题: 临床医学
题名:
NF-kappaB mediates the survival of human bronchial epithelial cells exposed to cigarette smoke extract
作者: 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
发表日期: 2008-09-23
DOI: 10.1186/1465-9921-9-66
卷: 9
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Respiratory System
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
项目资助者: American Lung Association (XL) ; Larson Endowment ; University of Nebraska Medical Center (SIR)
WOS记录号: WOS:000260432600001
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/56688
Appears in Collections:北京大学第三临床医学院_期刊论文

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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

Recommended Citation:
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.
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