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学科主题: 临床医学
题名:
Hydrogen Sulfide Suppresses Oxidized Low-density Lipoprotein (Ox-LDL)-stimulated Monocyte Chemoattractant Protein 1 generation from Macrophages via the Nuclear Factor kB ( NF- kB) Pathway*
作者: Du, Junbao1; Huang, Yaqian1; Yan, Hui1; Zhang, Qiaoli1; Zhao, Manman1; Zhu, Mingzhu1; Liu, Jia1; Chen, Stella X.3; Bu, Dingfang2; Tang, Chaoshu4,5; Jin, Hongfang1
关键词: Hydrogen Sulfide ; Inflammation ; Macrophages ; NF-B ; Sulfhydryl
刊名: JOURNAL OF BIOLOGICAL CHEMISTRY
发表日期: 2014-04-04
DOI: 10.1074/jbc.M113.517995
卷: 289, 期:14, 页:9741-9753
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Biochemistry & Molecular Biology
研究领域[WOS]: Biochemistry & Molecular Biology
关键词[WOS]: FACTOR-KAPPA-B ; BLOOD MONONUCLEAR LEUKOCYTES ; HUMAN ENDOTHELIAL-CELLS ; SMOOTH-MUSCLE CELLS ; GENE-EXPRESSION ; MESANGIAL CELLS ; ALPHA KINASE ; ACTIVATION ; MCP-1 ; P65
英文摘要:

Background: The mechanisms by which H2S regulates inflammation remain unclear. Results: H2S inhibits NF-B p65 phosphorylation, nuclear translocation, DNA binding activity, and recruitment to MCP-1 promoter in ox-LDL-treated macrophages by targeting the free sulfhydryl group on cysteine 38 in p65. Conclusion: H2S inhibits macrophage inflammation by suppressing NF-B activation. Significance: These findings reveal mechanisms for regulation of NF-B pathway by H2S.

This study was designed to examine the role of hydrogen sulfide (H2S) in the generation of oxidized low-density lipoprotein (ox-LDL)-stimulated monocyte chemoattractant protein 1 (MCP-1) from macrophages and possible mechanisms. THP-1 cells and RAW macrophages were pretreated with sodium hydrosulfide (NaHS) and hexyl acrylate and then treated with ox-LDL. The results showed that ox-LDL treatment down-regulated the H2S/cystathionine--synthase pathway, with increased MCP-1 protein and mRNA expression in both THP-1 cells and RAW macrophages. Hexyl acrylate promoted ox-LDL-induced inflammation, whereas the H2S donor NaHS inhibited it. NaHS markedly suppressed NF-B p65 phosphorylation, nuclear translocation, DNA binding activity, and recruitment to the MCP-1 promoter in ox-LDL-treated macrophages. Furthermore, NaHS decreased the ratio of free thiol groups in p65, whereas the thiol reductant DTT reversed the inhibiting effect of H2S on the p65 DNA binding activity. Most importantly, site-specific mutation of cysteine 38 to serine in p65 abolished the effect of H2S on the sulfhydration of NF-B and ox-LDL-induced NF-B activation. These results suggested that endogenous H2S inhibited ox-LDL-induced macrophage inflammation by suppressing NF-B p65 phosphorylation, nuclear translocation, DNA binding activity, and recruitment to the MCP-1 promoter. The sulfhydration of free thiol group on cysteine 38 in p65 served as a molecular mechanism by which H2S inhibited NF-B pathway activation in ox-LDL-induced macrophage inflammation.

语种: 英语
所属项目编号: 2011CB503904 ; 2012CB517806 ; 2013CB933801 ; 30901620 ; 31130030 ; 30821001 ; 7122184 ; 7121014
项目资助者: Major Basic Research Development Program of People&prime ; s Republic of China ; National Natural Science Foundation of China ; Beijing Natural Science Foundation
WOS记录号: WOS:000333807000026
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/54148
Appears in Collections:北京大学第一临床医学院_儿科_期刊论文

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作者单位: 1.Minist Educ, Key Lab Mol Cardiol, Beijing 100191, Peoples R China
2.Peking Univ, Hosp 1, Cent Lab, Beijing 100034, Peoples R China
3.Peking Univ, Dept Pediat, Hosp 1, Beijing 100034, Peoples R China
4.Univ Calif San Diego, Dept Biochem & Cellular Biol, La Jolla, CA 92092 USA
5.Peking Univ, Hlth Sci Ctr, Dept Physiol & Pathophysiol, Beijing 100191, Peoples R China

Recommended Citation:
Du, Junbao,Huang, Yaqian,Yan, Hui,et al. Hydrogen Sulfide Suppresses Oxidized Low-density Lipoprotein (Ox-LDL)-stimulated Monocyte Chemoattractant Protein 1 generation from Macrophages via the Nuclear Factor kB ( NF- kB) Pathway*[J]. JOURNAL OF BIOLOGICAL CHEMISTRY,2014,289(14):9741-9753.
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