• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

转化生长因子β1调节血管紧张素II诱导的血管平滑肌钙内流。

Transforming growth factor beta 1 modulates angiotensin II-induced calcium influx in vascular smooth muscle.

作者信息

Zhu Z, Tepel M, Neusser M, Zidek W

机构信息

Medizinische Universitäts-Poliklinik, University of Münster, Germany.

出版信息

Eur J Clin Invest. 1995 May;25(5):317-21. doi: 10.1111/j.1365-2362.1995.tb01708.x.

DOI:10.1111/j.1365-2362.1995.tb01708.x
PMID:7628518
Abstract

The modulatory effects of transforming growth factor beta 1 (TGF beta 1) on the angiotensin II (Ang II)-induced increase in cytosolic free calcium concentration ([Ca2+]i) were investigated in vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). [Ca2+]i in VSMC was measured using the fluorescent dye fura-2. When TGF beta 1 was applied 30s prior to Ang II, the Ang II-induced [Ca2+]i increase was significantly enhanced in VSMC from SHR (P < 0.05 compared to control), whereas after the preincubation with TGF beta 1 for 30 min, the Ang II-induced [Ca2+]i increase was significantly reduced in VSMC from both strains. Using the manganese-quenching technique, it was confirmed that short-term exposure to TGF beta 1 enhanced the Ang II-induced trans-plasma-membrane calcium influx in SHR. The inhibition of protein kinase C by calphostin C abolished the stimulatory effect of TGF beta 1 on the Ang II-induced [Ca2+]i increase. It is concluded that TGF beta 1 modulates the Ang II-induced calcium handling in VSMC.

摘要

研究了转化生长因子β1(TGFβ1)对自发性高血压大鼠(SHR)和正常血压的Wistar-Kyoto大鼠(WKY)血管平滑肌细胞(VSMC)中血管紧张素II(Ang II)诱导的胞质游离钙浓度([Ca2+]i)升高的调节作用。使用荧光染料fura-2测量VSMC中的[Ca2+]i。当在Ang II之前30秒应用TGFβ1时,SHR的VSMC中Ang II诱导的[Ca2+]i升高显著增强(与对照组相比,P < 0.05),而在用TGFβ1预孵育30分钟后,两种品系的VSMC中Ang II诱导的[Ca2+]i升高均显著降低。使用锰淬灭技术证实,短期暴露于TGFβ1可增强SHR中Ang II诱导的跨质膜钙内流。钙磷蛋白C对蛋白激酶C的抑制消除了TGFβ1对Ang II诱导的[Ca2+]i升高的刺激作用。得出结论,TGFβ1调节VSMC中Ang II诱导的钙处理。

相似文献

1
Transforming growth factor beta 1 modulates angiotensin II-induced calcium influx in vascular smooth muscle.转化生长因子β1调节血管紧张素II诱导的血管平滑肌钙内流。
Eur J Clin Invest. 1995 May;25(5):317-21. doi: 10.1111/j.1365-2362.1995.tb01708.x.
2
Abnormal regulation of transforming growth factor-beta receptors on vascular smooth muscle cells from spontaneously hypertensive rats by angiotensin II.血管紧张素II对自发性高血压大鼠血管平滑肌细胞上转化生长因子-β受体的异常调节
Hypertension. 1998 Feb;31(2):672-7. doi: 10.1161/01.hyp.31.2.672.
3
The effects of angiotensin II, endothelin-1, and protein kinase C inhibitor on DNA synthesis and intracellular calcium mobilization in vascular smooth muscle cells from young normotensive and spontaneously hypertensive rats.血管紧张素II、内皮素-1和蛋白激酶C抑制剂对正常血压年轻大鼠和自发性高血压大鼠血管平滑肌细胞DNA合成及细胞内钙动员的影响
Am J Hypertens. 1999 Dec;12(12 Pt 1-2):1243-51. doi: 10.1016/s0895-7061(99)00158-2.
4
Role of endogenous angiotensin II in the increased expression of growth factors in vascular smooth muscle cells from spontaneously hypertensive rats.内源性血管紧张素II在自发性高血压大鼠血管平滑肌细胞中生长因子表达增加中的作用
J Cardiovasc Pharmacol. 2001 Jan;37(1):108-18. doi: 10.1097/00005344-200101000-00013.
5
Transforming growth factor-beta1 modulates angiotensin II-induced calcium release in vascular smooth muscle cells from spontaneously hypertensive rats.
J Hypertens. 2000 Jun;18(6):733-42. doi: 10.1097/00004872-200018060-00011.
6
Role of calcium influx and intracellular calcium stores in angiotensin II-mediated calcium hyper-responsiveness in smooth muscle from spontaneously hypertensive rats.钙内流和细胞内钙储备在自发性高血压大鼠平滑肌中血管紧张素 II 介导的钙高反应性中的作用
J Hypertens. 1997 Dec;15(12 Pt 1):1431-9. doi: 10.1097/00004872-199715120-00010.
7
Mesenteric vascular smooth muscle cells from spontaneously hypertensive rats display increased calcium responses to angiotensin II but not to endothelin-1.自发性高血压大鼠的肠系膜血管平滑肌细胞对血管紧张素II的钙反应增强,但对内皮素-1的反应无增强。
J Hypertens. 1994 Jun;12(6):663-73.
8
Different calcium storage pools in vascular smooth muscle cells from spontaneously hypertensive and normotensive Wistar-Kyoto rats.自发性高血压和正常血压的Wistar-Kyoto大鼠血管平滑肌细胞中不同的钙储存池。
J Hypertens. 1994 May;12(5):533-8.
9
Extracellular signal-regulated kinase pathway is involved in basic fibroblast growth factor effect on angiotensin II-induced Ca(2+) transient in vascular smooth muscle cell from Wistar-Kyoto and spontaneously hypertensive rats.细胞外信号调节激酶通路参与碱性成纤维细胞生长因子对Wistar-Kyoto大鼠和自发性高血压大鼠血管平滑肌细胞中血管紧张素II诱导的Ca(2+)瞬变的影响。
Hypertension. 2000 Jan;35(1 Pt 1):61-7. doi: 10.1161/01.hyp.35.1.61.
10
Troglitazone inhibits growth and improves insulin signaling by suppression of angiotensin II action in vascular smooth muscle cells from spontaneously hypertensive rats.曲格列酮通过抑制自发性高血压大鼠血管平滑肌细胞中血管紧张素II的作用来抑制生长并改善胰岛素信号传导。
Atherosclerosis. 2002 Aug;163(2):229-39. doi: 10.1016/s0021-9150(02)00014-x.

引用本文的文献

1
Calcium input potentiates the transforming growth factor (TGF)-beta1-dependent signaling to promote the export of inorganic pyrophosphate by articular chondrocyte.钙内流增强转化生长因子 (TGF)-β1 依赖性信号转导,促进关节软骨细胞无机焦磷酸盐的输出。
J Biol Chem. 2011 Jun 3;286(22):19215-28. doi: 10.1074/jbc.M110.175448. Epub 2011 Apr 6.
2
A role for angiotensin II type 1 receptors on bone marrow-derived cells in the pathogenesis of angiotensin II-dependent hypertension.血管紧张素 II 型 1 受体在骨髓来源细胞中在血管紧张素 II 依赖性高血压发病机制中的作用。
Hypertension. 2010 Jan;55(1):99-108. doi: 10.1161/HYPERTENSIONAHA.109.144964. Epub 2009 Dec 7.
3
Uncoupling of ER-mitochondrial calcium communication by transforming growth factor-beta.
转化生长因子-β导致内质网-线粒体钙信号通讯解偶联
Am J Physiol Renal Physiol. 2008 Nov;295(5):F1303-12. doi: 10.1152/ajprenal.90343.2008. Epub 2008 Jul 23.
4
Transforming growth factor beta in cardiovascular development and function.转化生长因子β在心血管发育与功能中的作用
Cytokine Growth Factor Rev. 2003 Oct;14(5):391-407. doi: 10.1016/s1359-6101(03)00044-3.