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Signal transducers and activators of transcription 3 mediates up-regulation of angiotensin Ⅱ-induced tissue inhibitor of metalloproteinase-1 expression in cultured human senescent fibroblasts

ISSN号：0366-6999
期刊名称：《中华医学杂志：英文版》
时间：0
分类：Q51[生物学—生物化学]
作者机构：[1]Department of Nephrology, General Hospital of People＇s Liberation Army, Beijing 100853, China, [2]Department of Gastroenterology, Fourth Military Medical University, Xi＇an 710032, China, [3]Institute of Genome Research, Tsinghua University, Beijing 100084, China
相关基金：This work was supported by grants from the Creative Research Group Fund of the Natural Science Foundation of China （No. 30121005）, the National Science Foundation of China （No. 30370559）, the Medical Health Research Fund of People＇s Liberation Army of China （No. 04T6003）, and the Major Basic Project of China （973）（No.G2000057000）.Acknowledgement： We would like to give our thanks to Dr. Jennifer Rubins Grandis （University of Pittsburgh） and Dr. FU Xin-yuan （Yale University School of Medicine） for their generous gifts of U6-STAT3-S （STAT3 sense） and U6-STAT3-AS （STAT3 antisense）, and of pMS1 plasmid and STAT3 mutant plasmid, respectively. We are also grateful to Dr. HE You-wen （Duke University） for his critical examination and helpful suggestions on this manuscript.

作者： WANG Xiao-dan[1,2], CHEN Xiang-mei[1], WANG Jian-zhong[1], HONG Quan[1], FENG Zhe[1], FU Bo[1], ZHOU Feng[1], WANG Feng-yang[3], FAN Dai-ming[2]

关键词：信号转导, 活化剂, 血管紧缩素Ⅱ, 金属蛋白酶-1, STAT3 protein, human, tissue inhibitor of metalloproteinase-1, angiotensin Ⅱ, aging, fibroblasts

中文摘要：

Backgroud 血管收缩素Ⅱ(Ang Ⅱ) ， renin-angiotensinsystem (地岬) 的一个主要受动器并且在老化纸巾增加了，能经由 theG-protein-coupled Ang Ⅱ受体类型Ⅰ(AT1 ) 刺激 JAK/STAT 小径并且导致信号变换器的原子 translocation 和抄写(STAT ) 的使活跃之物。为了推进，在老化探索 Ang Ⅱ的角色，我们在人的 replicative 上检验了 Ang Ⅱ的效果衰老的双成纤维细胞 WI-38 房间。方法人的衰老的 WI-38 房间与 Ang Ⅱ，受体对手 PD123319， valsartan， STAT3 感觉原生质标志，或 STAT3 反感觉原生质被孵化标志。方法被使用 includingelectrophoretic 活动性移动试金(EMSA ) ，西方的污点， transfection，并且激光扫描共焦的显微镜学。有教养的人的衰老的 WI-38 房间组成地表示了 metalloproteinase-1 (TIMP-1 ) 的织物禁止者，这被发现的结果，和 Ang Ⅱ在时间依赖者和剂量依赖者礼貌导致了 TIMP-1 蛋白质表示。Ang Ⅱ在两时间也导致了 STAT-DNA 有约束力的活动 -- 并且剂量依赖者礼貌。并且超级移动试金证明导致 sis 因素(SIF ) 乐队包含了 STAT3 蛋白质。STAT3 反感觉 oligonucleotides 能禁止两项 Ang Ⅱ - inducedSTAT3-DNA 绑定活动以及 TIMP-1 表示。结论 Ang Ⅱ通过激活 STAT3 的起来调整 TIMP-1expression 能在人的衰老的房间表明小径，显示那条 Ang Ⅱ - STAT3-TIMP-1 小径可以在老化纸巾涉及硬化的机制。

英文摘要：

Backgroud Angiotensin Ⅱ （Ang Ⅱ）, a principal effector of renin-angiotensin system （RAS） and increased in aging tissues, can stimulate JAK/STAT pathway via the G-protein-coupled Ang Ⅱ receptor type Ⅰ （AT1） and induce nuclear translocation of signal transducers and activators of transcription （STAT）. To further explore the role of Ang Ⅱ in aging, we examined the effect of Ang Ⅱ on human replicative senescent diploid fibroblast WI-38 cells.

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