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|本期目录/Table of Contents|

NF-κB在铁负荷过低上调炎症因子中的作用

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2011年第2期
页码:
205-208
栏目:
基础研究
出版日期:
2010-12-10

文章信息/Info

Title:
Effect of nuclear factor (NF)-κB on induction of EMMPRIN by excessive low iron load in macrophages and foam cells
作者:
范虞琪1; 魏立2; 王君2
1.上海交通大学医学院新华医院心内科，上海 200092；2.上海伤骨科研究所，上海 200025
Author(s):
FAN Yu-qi1;  Wei Li2;  Wang Jun2
1.Department of Cardiology, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200092, China; 2.Shanghai Institute of Traumatology and Orthopedics, Shanghai 200025, China
关键词:
铁负荷过低; 细胞外基质金属蛋白酶诱导因子; 核转录因子-κB; 动脉粥样硬化
Keywords:
excessive low iron load;  extracellular matrix metalloproteinase inducer;  nuclear factor-κB;  atherosclerosis
分类号:
Q559
DOI:
-
文献标识码:
A
摘要:
目的: 探讨核转录因子(NF)-κB在铁负荷过低上调巨噬细胞、泡沫细胞炎症因子反应中的作用。方法： 将巨噬细胞和泡沫细胞给予NF-κB抑制剂预处理，加入或不加入铁离子鳌合剂去铁胺(DFO)继续培养24 h，用Western blot测定细胞中细胞外基质金属蛋白酶诱导因子（EMMPRIN）蛋白的表达。于巨噬细胞和泡沫细胞中加入DFO刺激，用Western blot测定细胞核中NF-κB p65蛋白的表达。将巨噬细胞和泡沫细胞给予p38 MAPK信号通路抑制剂或视黄醛x受体（RXR）的天然配体预处理，加入DFO刺激，用Western blot测定细胞核中NF-κB p65蛋白的表达。结果： NF-κB抑制剂可抑制DFO对巨噬细胞、泡沫细胞中EMMPRIN上调的作用。DFO可促进巨噬细胞、泡沫细胞细胞核中NF-κB p65蛋白的表达。p38 MAPK通路抑制剂或RXR配体可抑制DFO对NF-κB p65蛋白水平上调的作用。结论： NF-κB 参与了铁负荷过低上调巨噬细胞和泡沫细胞中EMMPRIN表达的过程。RXR配体对铁负荷过低上调炎症反应的抑制作用，同其抑制NF-κB激活有关。
Abstract:
AIM: To investigate the effect of NF-κB on the induction of EMMPRIN by excessive low iron load in macrophages and foam cells. METHODS: Thp-1 derived macrophages and foam cells were pre-treated with NF-κB inhibitor and then were stimulated with/without desferrioxamine (DFO) for 24 h. EMMPRIN expression was assayed by Western blot. Cells were stimulated with DFO for different time periods and nuclear NF-κB p65 protein levels were then assayed by Western blot. Cells were pre-treated with p38 MAPK inhibitors or RXR ligand and nuclear NF-κB p65 protein levels were assayed again by Western blot. RESULTS: NF-κB inhibitor blocked the induction of EMMPRIN by DFO stimulation, DFO enhanced nuclear NF-κB p65 protein levels in macrophages and foam cells and p38 MAPK inhibitor and RXR ligand significantly blocked DFO upregulation of NF-κB p65. CONCLUSION: NF-κB is involved not only in the excessive low iron load upregulation of EMMPRIN expression, but also in the RXR ligand downregulation of inflammatory factor in macrophages and foam cells.

参考文献/References

[1]Thurberg BL, Collins T. The nuclear factor-kappa B/inhibitor of kappa B autoregulatory system and atherosclerosis［J］. Curr Opin Lipidol, 1998, 9(5):387-396.

[2]范虞琪，何奔，王斌尧，等. 铁离子螯合剂去铁胺对巨噬细胞、泡沫细胞细胞外基质金属蛋白酶诱导因子表达的影响［J］.心脏杂志， 2009， 21（5）：601-605.

[3]范虞琪，何奔，王斌尧，等. 铁离子螯合剂去铁胺上调巨噬细胞、泡沫细胞细胞外基质金属蛋白酶诱导因子表达的机理探讨［J］.心脏杂志， 2009， 21（6）：757-760，769.

[4] Schmidt R, Bultmann A, Ungerer M, et al. Extracellular matrix metalloproteinase inducer regulates matrix metalloproteinase activity in cardiovascular cells: implications in acute myocardial infarction［J］. Circulation, 2006, 113(6):834-841.

[5]Huang Z, Wang C, Wei L, et al. Resveratrol inhibits EMMPRIN expression via P38 and ERK1/2 pathways in PMA-induced THP-1 cells［J］. Biochem Biophys Res Commun, 2008, 374(3):517-521.

[6]Lim M, Martinez T, Jablons D, et al. Tumor-derived EMMPRIN (extracellular matrix metalloproteinase inducer) stimulates collagenase transcription through MAPK p38［J］. FEBS Lett, 1998, 441(1):88-92.

[7]Hata K, Andoh A, Shimada M, et al. IL-17 stimulates inflammatory responses via NF- κB and MAP kinase pathways in human colonic myofibroblasts［J］. Am J Physiol Gastrointest Liver Physiol, 2002, 282(6):G1035-G1044.

[8]Marie C, Arielle M, Luise H, et al. Involvement of MAPK pathway in TNF-α -induced MMP-9 expression in human trophoblastic cells Molecular［J］. Human Reproduction, 2006, 12(4):225-232.

[9]Claudel T, Leibowitz MD, Fievet C, et al. Reduction of atherosclerosis in apolipoprotein E knockout mice by activation of the retinoid X receptor［J］. Proc Natl Acad Sci U S A, 2001, 98(5):2610-2615.

[10]Lalloyer F, Fievet C, Lestavel S, et al. The RXR agonist bexarotene improves cholesterol homeostasis and inhibits atherosclerosis progression in a mouse model of mixed dyslipidemia［J］. Arterioscler Thromb Vasc Biol, 2006, 26(12):2731-2737.

[11]Na S, Kim H, Lee S, et al. IkappaBbeta interacts with the retinoid X receptor and inhibits retinoid-dependent transactivation in lipopolysaccharide-treated cells［J］. J Biol Chem, 1998, 273(6):3212-3215.

[12]Razny U, Wator L, Polus A, et al. Hepatocyte RXR alpha deletion in mice leads to inhibition of angiogenesis［J］. Genes Nutr, 2009, 4(1):69-72.

备注/Memo

备注/Memo:
收稿日期：2010-05-26.作者简介：范虞琪，住院医师，博士Email：moricizine@gmail.com
更新日期/Last Update: 2010-12-10