[1]石向东,李志梁,吴宏超,等.尾加压素刺激血管内皮细胞分泌肾上腺髓质素的机制[J].南方医科大学学报,2005,(07):791-793.
 SHI Xiang-dong,LI Zhi-liang,WU Hong-chao,et al.Mechanism of urotensin Ⅱ-stimulated adrenomedullin secretion in human vascular endothelial cells[J].Journal of Southern Medical University,2005,(07):791-793.
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尾加压素刺激血管内皮细胞分泌肾上腺髓质素的机制()
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《南方医科大学学报》[ISSN:1673-4254/CN:44-1627/R]

卷:
期数:
2005年07期
页码:
791-793
栏目:
出版日期:
2005-07-01

文章信息/Info

Title:
Mechanism of urotensin Ⅱ-stimulated adrenomedullin secretion in human vascular endothelial cells
作者:
石向东1 李志梁1 吴宏超1 王同汉1 傅强1 严全能1 唐朝枢2
1. 南方医科大学珠江医院心内科, 广东, 广州, 510282;
2. 北京大学第一医院心血管研究所, 北京, 100034
Author(s):
SHI Xiang-dong1 LI Zhi-liang1 WU Hong-chao1 WANG Tong-han1 Fu Qiang1 YAN Quan-neng1 TANG Chao-shu2
1. Department of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China;
2. Institute of Cardiovascular Disease, First Affiliated Hospital, Peking University, Beijing 100034, China
关键词:
内皮细胞尾加压素肾上腺髓质素信号转导
Keywords:
endothelial cellsurotensinadrenomedullinsignal transduction
分类号:
R-33
摘要:
目的 研究人尾加压素(UⅡ)刺激人血管内皮细胞(HVEC)分泌肾上腺髓质素(Adm)的机制。方法 以不同浓度的UⅡ(10-10、10-9、10-8、10-7mol/L)刺激培养的HVEC,放射免疫法测定其分泌Adm的量,以及不同的细胞信号转导阻滞剂(丝裂素活化蛋白激酶阻断剂PD98059、钙调素依赖性蛋白激酶阻断剂W7、P38蛋白激酶抑制剂SB202190、钙通道阻断剂nicardipine、蛋白激酶C阻断剂H7及钙调神经磷酸酶抑制剂环孢霉素)对其分泌的影响。结果 UⅡ可促进HVEC分泌Adm,且呈时间和浓度依赖性。各组与对照组之间有显著差别。PD98059、W7、SB202190及nicardipine均能抑制UⅡ刺激的HVEC对Adm的分泌,其抑制率分别为67%(P<0.01)、77%(P<0.01)、23%(P<0.05)、24%(P<0.05)。而H7、CsA对UⅡ刺激HVEC分泌Adm无显著影响(P>0.05)。结论 UⅡ能刺激HVEC分泌Adm,其机制与Ca2+、MAPK、CaMPK及P38信号转导通路介导有关。
Abstract:
Objective To study the mechanism of urotensin Ⅱ( UⅡ)-stimulated adrenomedullin secretion in human vascular endothelial cells. Methods In cultured human vascular endothelial cells (HEVCs),different concentrations of UⅡ was used to stimulate the secretion of Adm,and different inhibitors were used to study the changes in the secretion after block of different signal transduction pathways.The contents of Adm in the medium were detected with radioimmunoassay. Results UⅡ-stimulated Adm secretion in the HEVCs in a time- and concentration-dependent manner.Adm contents of the treatment groups were comparable with that of the control group (P<0.05 ),and the secretion of Adm could be inhibited by the inhibitor of extracellular signal-regulated protein kinases (PD098059),p38 kinase inhibitor (SB202190),calmodulin inhibitor (W7) and Ca2+ inhibitor (nicardipine)(P<0.05),but calcineurin inhibitor and protein kinase C inhibitor (H7) had no such effect (P>0.05). Conclusion Ca2+,MAPK,CaM-PK and p38 signal transduction pathways may play major roles in UⅡ-stimulated cecretion of Adm in HVECs.

参考文献/References:

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备注/Memo

备注/Memo:
收稿日期:2005-1-6。
基金项目:国家重大发展基础研究项目(973)子课题(G200056905)
作者简介:石向东(1975- ),男,1999年毕业于华北煤碳医学院,现为南方医科大学在读硕士研究生,主治医师
通讯作者:李志梁,电话:020-61643161
更新日期/Last Update: 1900-01-01