Amplification of angiotensin II signaling in cardiac myocytes by adenovirus-mediated overexpression of the AT1 receptor.
Amplification of angiotensin II signaling in cardiac myocytes by adenovirus-mediated overexpression of the AT1 receptor.
复制标题
通过腺病毒介导的 AT1 受体过度表达来放大心肌细胞中的血管紧张素 II 信号传导。
DOI：
10.1111/j.1749-6632.1999.tb09221.x
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发表时间：
1999
影响因子：
5.2
通讯作者：
Baker,KM
中科院分区：
文献类型：
--
作者：
Booz,GW;Carl,LL;Baker,KM
摘要：低水平的血管紧张素受体（at1）会使研究心肌细胞中由该受体介导的生长相关信号转导事件在技术上变得困难。本研究的目的是建立腺病毒表达系统是否可以增加新生大鼠心室肌细胞质膜at1受体的数量，从而放大该受体激活的信号通路。表达at1受体的腺病毒感染心肌细胞表现出配体结合增加。就激动剂诱导的内化，以及与MAPK激活和蛋白酪氨酸磷酸化事件的偶联而言，过表达受体的功能似乎与内源性受体相似。此外，腺病毒介导的at1受体的过表达导致血管紧张素II细胞内信号的扩增。总之，腺病毒介导的血管紧张素II受体的过表达似乎是研究这种激素在心肌细胞中激活的信号转导事件和揭示这种受体类型与肥大生长和基因表达模式耦合的分子手段的有用策略。
Abstract:Low levels of AT1receptor can make studying the growth‐related signal transduction events mediated by this angiotensin II receptor in cardiac myocytes technically difficult. The purpose of the present study was to establish whether an adenovirus expression system could be used to increase the number of plasma membrane AT1receptors in neonatal rat ventricular myocytes, thereby amplifying the signaling pathways activated by this receptor. Cardiac myocytes infected with adenovirus expressing the AT1receptor exhibited increased ligand binding. The overexpressed receptor appeared to function like the endogenous receptor, in regard to agonist‐induced internalization, as well as coupling to MAPK activation and protein tyrosine phosphorylation events. In addition, adenovirus‐mediated overexpression of the AT1receptor resulted in the amplification of angiotensin II intracellular signaling. In conclusion, adenovirus‐mediated overexpression of angiotensin II receptors appears to be a useful strategy for studying the signal transduction events activated by this hormone in cardiac myocytes and for unraveling the molecular means by which this receptor type couples to a hypertrophic pattern of growth and gene expression.