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|本期目录/Table of Contents|

肿瘤坏死因子超家族基因在慢性心力衰竭外周血单核细胞的表达(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2005年第5期
页码:
453-457
栏目:
临床研究
出版日期:
2005-10-05

文章信息/Info

Title:
Gene expression of tumor necrosis factor superfamily in peripheral blood mononuclear cells during chronic heart failure
作者:
顾水明1;  魏 盟1;  张昀昀1;  邵 君3;  李 奇3;  吴宗贵2
1. 上海交通大学附属第六人民医院心内科, 上海 200233; 2. 第二军医大学附属长征医院心内科，上海 200003；3.生物芯片上海国家工程研究中心,上海 201203
Author(s):
GU Shuiming1; WEI Meng1;  ZHANG Yunyun1;  SHAO Jun3;  LI Qi3; WU Zonggui2
1. Department of Cardiology,Affiliated No 6 Hospital,Shanghai Jiaotong University, Shanghai, 200233； 2. Department of Cardiology, Changzheng Hospital,Second Military Medical University,Shanghai 200003，China；3. Shanghai National Engineering Center for Bi
关键词:
心力衰竭; 细胞因子;  白细胞; 基因表达
Keywords:
heart failure;  cytokines;  leukocytes;  gene expression
分类号:
R541.6
DOI:
-
文献标识码:
A
摘要:
目的 应用基因芯片技术分析比较慢性心力衰竭(CHF)患者和健康对照组外周血单核细胞(PBMC)中细胞因子和其它炎症相关基因表达差异，以识别CHF细胞因子网络的不平衡。方法 分别抽提CHF和健康对照组PBMC总RNA并纯化mRNA，反转录合成单链、双链cDNA后，体外转录合成cRNA。分别用cy3dCTP和cy5dCTP标记对照和CHF组cRNA。将基因芯片和杂交探针变性后杂交、洗涤。用基因芯片扫描仪进行图像扫描，ImaGene 3.0软件分析cy3、cy5两种荧光信号的强度和比值。结果 cDNA表达谱芯片中含365个炎性细胞因子相关基因，其中CHF组上调34个基因，下调2个。上调基因包括肿瘤坏死因子(TNF)超家族成员，趋化因子/趋化因子受体，转化生长因子超家族成员等。TNF超家族成员中，淋巴毒素(LTB)、TNF超家族成员5、7、10，TNF受体超家族成员13b，TNF相关凋亡诱导配体受体4(TRAILR4)在CHF组均上调。而 TNF受体超家族成员10C (TRAILR3)在CHF显著下调。结论 CHF与正常人PBMC细胞因子相关基因的表达有显著差异，CHF存在细胞因子网络的不平衡；尤其是多个TNF超家族基因的高表达可能在CHF发生发展中起着重要作用。
Abstract:
AIM To investigate the gene expression difference of cytokines and related mediators in peripheral blood mononuclear cells (PBMC) between chronic heart failure(CHF) patients and healthy subjects， and identify the imbalance in the cytotokine network in CHF. METHODS Total RNA was extracted from PBMCs of CHF patients and healthy subjects and transcripted to single, two stranded cDNA and cRNA. Two probes were labled with cy3 and cy5 fluorescence, mixed and hybridized with the gene chip. The hybridizing signals were deetected by laser scanner and analysed with and ImaGene 3.0 software. RESULTS Among the 365 cytokines and related mediator genes in the gene chip, 34 were upregulated and 2 downregulated in CHF patients. The regulated genes included several members of tumor necrosis factor (TNF) superfamily， chemokines/receptors, members of the transforming growth factor superfamily. Of the TNF superfamily members, lymphotoxin，TNFSF5，TNFSF7，TNFSF10，TNFRSF13B，and TRAILR4 were upregulated, while TNFRSF10C(TRAILR3) was downregulated. CONCLUSION There are significant differences in gene expressions of cytokines and related mediators in PBMCs between CHF patients and healthy subjects and the imbalance in the cytokine network in CHF. In particular, the enhanced expression of several members in the TNF superfamily may play a potential pathogenic role in CHF.

参考文献/References

［1］ Blum A, Miller H. Pathophysiological role of cytokines in congestive heart failure［J］. Annu Rev Med, 2001, 52: 15-27.

［2］ Li YY, Feng YQ, Kadokami T, et al. Myocardial extracellular matrix remodeling in transgenic mice overexpressing tumor necrosis factor alpha can be modulated by antitumor necrosis factor alpha therapy［J］. Proc Natl Acad Sci USA, 2000, 97: 12746-1275I.

［3］ 臧益民，臧伟进，王晓明．心力衰竭的病理生理机制及治疗概述［J］. 心脏杂志，2002，14(5)：417-419．

［4］ Coletta AP, Clark AL, Banarjee P, et al. Clinical trials update: RENEWAL (RENAISSANCE and RECOVER) and ATTACH［J］. Eur J Heart Fail, 2002, 4(4): 559-561.

［5］ 王晓明，李源，李慧，等．心力衰竭患者血清中TNFα、IL1及IL6的变化及培哚普利对其影响［J］. 心脏杂志，2002，14(4)：318-322．

［6］ Damas JK, Lars G, Aass H, et al. Enhanced gene expression of chemokines and their corresponding receptors in mononuclear blood cells in chronic heart failure modulatory effects of intravenous immunoglobulin［J］. J Am Coll Cardiol, 2001, 38(1): 187-193.

［7］ Damas JK, Eiken HG, Qie E, et al. Myocardial expression of CC CXCchemokines and their receptors in human endstage heart failure［J］. Cardiovasc Res, 2000, 47: 778-787.

［8］ Pan G, Ni J, Wei YF , et al. An antagonist decoy receptor and a death domaincontaining receptor for TRAIL［J］. Science, 1997, 277: 815-818.

［9］ Kang PM, Izumo S. Apoptosis and heart failure:a critical review of the literature［J］. Cir Res, 2000, 86: 1107-1113.

［10］Nelson DP, Setser E, Hall DG, et al. Proinflammatory consequences of transgenic fas ligand expression in the heart［J］. J Clin Invest, 2000, 105: l 199-1208.

备注/Memo

备注/Memo:
收稿日期：2005-05-08.
更新日期/Last Update: 2010-01-05