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学科主题: 临床医学
题名:
Fenoterol inhibits LPS-induced AMPK activation and inflammatory cytokine production through beta-arrestin-2 in THP-1 cell line
作者: Wang, Wei1,4; Zhang, Yuan1; Xu, Ming2,3; Zhang, You-Yi2,3; He, Bei1
关键词: beta(2)-adrenergic receptor ; Fenoterol ; AMPK ; beta-arrestin-2 ; Lipopolysaccharide ; THP-1 cell line
刊名: BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
发表日期: 2015-06-26
DOI: 10.1016/j.bbrc.2015.04.097
卷: 462, 期:2, 页:119-123
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Biochemistry & Molecular Biology ; Biophysics
研究领域[WOS]: Biochemistry & Molecular Biology ; Biophysics
关键词[WOS]: KAPPA-B ACTIVATION ; PROTEIN-KINASE ; IL-6 PRODUCTION ; BETA-ARRESTIN ; CARDIAC FIBROBLASTS ; LUNG-DISEASE ; TNF-ALPHA ; P38 MAPK ; RECEPTOR ; PATHWAY
英文摘要:

The AMP-activated protein kinase (AMPK) pathway is involved in regulating inflammation in several cell lines. We reported that fenoterol, a beta(2)-adrenergic receptor (beta(2)-AR) agonist, had anti-inflammatory effects in THP-1 cells, a monocytic cell line. Whether the fenoterol anti-inflammatory effect involves the AMPK pathway is unknown. In this study, we explored the mechanism of beta(2)-AR stimulation with fenoterol in a lipopolysaccharide (LPS)-induced inflammatory cytokine secretion in THP-1 cells. We studied whether fenoterol and beta-arrestin-2 or AMPK alpha l subunit knockdown could affect LPS-induced AMPK activation, nuclear factor-kappa B (NF-kappa B) activation and inflammatory cytokine secretion. LPS-induced AMPK activation and interleukin 1 beta (IL-1 beta) release were reduced with fenoterol pretreatment of THP-1 cells. SiRNA knockdown of beta-arrestin-2 abolished the fenoterol inhibition of LPS-induced AMPK activation and interleukin 1 beta (IL-1 beta) release, thus beta-arrestin-2 mediated the anti-inflammatory effects of fenoterol on LPS-treated THP-1 cells. In addition, siRNA knockdown of AMPK alpha 1 significantly attenuated the LPS-induced NF-kappa B activation and IL-1 beta release, so AMPKal was a key signaling molecule involved in LPS-induced inflammatory cytokine production. These results suggested the beta(2)-AR agonist fenoterol inhibited LPS-induced AMPK activation and IL-1 beta release via beta-arrestin-2 in THP-1 cells. The exploration of these mechanisms may help optimize therapeutic agents targeting these pathways in inflammatory diseases. (C) 2015 Elsevier Inc. All rights reserved.

语种: 英语
所属项目编号: 81270097 ; 7112745 ; 20090001110093
项目资助者: National Natural Science Foundation of China ; Beijing Natural Science Foundation ; Ph.D. Programs Foundation of Ministry of Education of China
WOS记录号: WOS:000356118200006
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/50174
Appears in Collections:北京大学第三临床医学院_呼吸内科_期刊论文

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作者单位: 1.Peking Univ, Dept Resp Med, Hosp 3, Beijing 100871, Peoples R China
2.Peking Univ, Dept Inst Vasc Med, Hosp 3, Beijing 100871, Peoples R China
3.Peking Univ, Beijing Key Lab Cardiovasc Receptors Res, Hosp 3, Key Lab Cardiovasc Mol Biol & Regulatory Peptides, Beijing 100871, Peoples R China
4.Peking Univ, Dept Infect Dis, Hosp 3, Beijing 100871, Peoples R China

Recommended Citation:
Wang, Wei,Zhang, Yuan,Xu, Ming,et al. Fenoterol inhibits LPS-induced AMPK activation and inflammatory cytokine production through beta-arrestin-2 in THP-1 cell line[J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS,2015,462(2):119-123.
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