我们的网站为什么显示成这样?

可能因为您的浏览器不支持样式,您可以更新您的浏览器到最新版本,以获取对此功能的支持,访问下面的网站,获取关于浏览器的信息:

|本期目录/Table of Contents|

ERK1/2信号通路在内皮微粒诱导人脐静脉内皮细胞ICAM-1表达中的作用(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2012年第2期
页码:
158-161,184
栏目:
基础研究
出版日期:
2012-04-25

文章信息/Info

Title:
Endothelial microparticle-induced ICAM-1 expression in human umbilical vein endothelial cells via ERK1/2 signaling pathway
作者:
陆永光符春晖严 华黄军章
(钦州市第二人民医院心内科,广西 钦州 535000)
Author(s):
LU Yong-guang FU Chun-hui YAN Hua HUANG Jun-zhang
(Department of Cardiology, Second People’s Hospital of Qinzhou, Qinzhou 535000, Guangxi, China)
关键词:
内皮细胞微粒脐静脉内皮细胞细胞外信号调节激酶1/2细胞间黏附分子-1
Keywords:
endothelial microparticles human umbilical vein endothelial cells extracellular signal-regulated kinases 1/2 intercellular adhesion molecule 1
分类号:
R54
DOI:
-
文献标识码:
A
摘要:
目的:探讨细胞外信号调节激酶1/2(ERK1/2)信号通路在内皮微粒(EMPs)诱导人脐静脉内皮细胞(HUVECs)表达细胞间黏附分子-1(ICAM-1)中的作用。方法:体外培养HUVECs,选取生长良好的第4~5代细胞,分为EMPs不同浓度作用组、EMPs不同时间作用组及ERKl/2特异性抑制剂组。应用蛋白免疫印迹法(Western blot)检测ICAM-1和磷酸化ERK1/2蛋白的表达。用实时荧光定量PCR(qRT-PCR)检测ICAM-1 mRNA的表达。结果:EMPs作用HUVECs后,ICAM-1 mRNA和其蛋白以及磷酸化ERK1/2蛋白的表达显著高于对照组,且呈浓度和时间依赖性的关系(均P<0.01);而ERKl/2特异性抑制剂PD98059对ICAM-1 mRNA和其蛋白以及磷酸化ERK1/2蛋白的表达,均有明显的抑制作用(均P<0.01)。结论:EMPs可诱导HUVECs中ICAM-1表达,其机制可能与激活ERK1/2信号通路有关。
Abstract:
AIM:To investigate the role of extracellular signal-regulated kinases 1/2 (ERK1/2) signaling pathway in endothelial microparticle (EMP)-induced expression of intercellular adhesion molecule 1 (ICAM-1) in human umbilical vein endothelial cells (HUVECs). METHODS: HUVECs were cultured in vitro and fourth to fifth generation cells were chosen for the test. HUVECs were incubated with EMPs at different concentrations and at different times or pretreated with inhibitors of ERK1/2 (PD98059) for 60 min before incubation. Protein expression of ERK1/2 and ICAM-1 was measured by Western blot in HUVECs. Quantitative real-time reverse transcriptase polymerase chain reaction (qRT-PCR) was used to analyze the mRNA expression of ICAM-1 in HUVECs. RESULTS: Exposure to EMPs caused a significant increase in mRNA and protein expressions of ICAM-1 and resulted in a rapid activation of ERK1/2 in a dose- and time-dependent manner (all P<0.01). The effect of EMPs was attenuated by PD98059 (all P<0.01). CONCLUSION: ERK1/2 signaling pathways are involved in EMP-induced expression of ICAM-1 in HUVECs.

参考文献/References

[1]Daleke DL.Regulation of transbilayer plasma membrane phospholipid asymmetry[J].J Lipid Res,2003,44(2):233-242.

[2]Amabile N,Boulanger CM,Guerin AP,et al.Circulating endothelial microparticles:a novel biomarker for cardiovascular death and cardiovascular events in end-stage-renal disease[J].Circulation,2009,120(18 Supplement):S1010.

[3]Chironi GN,Boulanger CM, Simon A,et al.Endothelial microparticles in diseases[J].Cell Tissue Res,2009,335(1):143-151.

[4]Wang JM,Huang YJ,Wang Y,et al.Increased circulating CD31+/CD42- microparticles are associated with impaired systemic artery elasticity in healthy subjects[J].Am J Hypertens,2007,20(9): 957-964.

[5]Chen CH,Song TY,Liang YC,et al.Acteoside and 6-O-acetylacteoside downregulate cell adhesion molecules induced by IL-1beta through inhibition of ERK and JNK in human vascular endothelial cells[J].J Agric Food Chem,2009,57(19):8852-8859.

[6]Terrisse AD,Puech N,Allart S,et al.Internalization of microparticles by endothelial cells promotes platelet/endothelial cell interaction under flow[J].J Thromb Haemost,2010,8(12):2810-2819.

[7]Dasgupta SK,Abdel-Monem H,Niravath P,et al.Lactadherin and clearance of platelet-derived microvesicles[J].Blood,2009,113(6):1332-1339.

[8]Bulut D,Tuns H,Mugge A.CD31+/Annexin V+ microparticles in healthy offsprings of patients with coronary artery disease[J].Eur J Clin Invest,2009,39(1):17-22.

[9]Jung KH,Chu K,Lee ST,et al.Risk of macrovascular complica-tions in type 2 diabetes mellitus: endothelial microparticle profiles[J].Cerebrovasc Dis,2011,31(5):485-493.

[10]陆永光,文 宏,苏 强,等.冠状动脉无复流患者内皮微粒变化的临床意义[J].中国急救医学, 2009,29(12):1070-1072.

[11]Maekawa Y,Ishikawa K,Yasuda O,et al.Klotho suppresses TNF-alpha-induced expression of adhesion molecules in the endothelium and attenuates NF-kappaB activation[J].Endocrine,2009,35(3):341-346.

[12]Galkina E,Ley K.Vascular adhesion molecules in atherosclerosis[J].Arterioscler Thromb Vasc Biol,2007,27(11):2292-2301.

[13]Jin YC,Kim CW, Kim YM,et al.Cryptotanshinone,a lipophilic compound of Salvia miltiorrriza root, inhibits TNF-alpha-induced expression of adhesion molecules in HUVEC and attenuates rat myocardial ischemia/reperfusion injury in vivo[J].Eur J Pharmacol,2009,614(1-3):91-97.

[14]Patti G,Chello M,Gatto L,et al.Short-term atorvastatin preload reduces levels of adhesion molecules in patients with acute coronary syndrome undergoing percutaneous coronary intervention. Results from the ARMYDA-ACS CAMs (Atorvastatin for Reduction of MYocardial Damage during Angioplasty-Cell Adhesion Molecules) substudy[J].J Cardiovasc Med (Hagerstown),2010,11(11):795-800.

[15]Yumoto H,Yamada M,Shinohara C,et al.Soluble products from Eikenella corrodens induce cell proliferation and expression of interleukin-8 and adhesion molecules in endothelial cells via mitogen-activated protein kinase pathways[J].Oral Microbiol Immunol,2007,22(1):36-45.

备注/Memo

备注/Memo:
收稿日期:2011-07-18.基金项目:广西壮族自治区卫生厅项目资助(Z2011103)作者简介: 陆永光,主治医师,博士 Email:evershine_lu@hotmail.com
更新日期/Last Update: 2012-04-01