VASCULAR SMOOTH MUSCL ADRENOCEPTOR FUNCTION & EXPRESSION
血管平滑肌肾上腺素受体功能
基本信息
- 批准号:2430745
- 负责人:
- 金额:$ 23.02万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:1994
- 资助国家:美国
- 起止时间:1994-07-05 至 1999-05-31
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
We have recently found that up to 4 different alpha-adrenoceptor (AR)
subtypes may be expressed by vascular smooth muscle cells (SMCs), that the
array of subtypes differs between artery and vein, and that certain
conditions may induce expression of a normally repressed subtype. Little
is known concerning regulation of expression of these different alphaARs
by SMCs. Moreover, all of the subtypes present may not mediate
contraction & their other SMC functions are unclear. While elevated
catecholamine activity promotes SMC growth & is a risk factor for
atherosclerosis & hypertensive hypertrophy little is known about how
alphaARs regulate SMC growth and the alphaAR subtypes involved. The
hypotheses to be tested are that: (1) A specific alphaAR subtype(s)
modulates SMC growth and expression of contractile & structural proteins,
thereby linking sympathetic state to SMC growth & differentiation. (2)
Fundamental signals in the vascular wall microenvironment, ie.,
catecholamines, oxygen and pressure-induced cell stretch regulate
expression of specific alphaAR subtypes. The following aims will be
examined in rat aorta SMCs in cell culture and in situ in the vascular
wall. Aim 1 examines the effect of stimulation of different alphaAR
subtypes on growth and gene expression (mRNA & protein) of alpha- and
beta-actin. Aim 2 determines the influence of stimulation of each subtype
on expression of the cognate & other alphaAR subtypes. Aim 3 investigates
regulation of alphaAR expression by oxygen. Aim 4 examines the effect of
cell stretch (pressure) on alphaAR expression. Aim 5 determines
involvement of changes in gene transcription rate (nuclear runoff), mRNA
stability, and DNA & protein synthesis in the altered expression of
actins, alphaAR subtypes and SMC growth induced by alphaAR stimulation,
tissue oxygen and cell stretch. Aim 6 tests the hypothesis that an O/2-
binding heme protein & sequences in the alpha1B-AR gene mediate hypoxia
stimulation of alpha1B expression. These studies will yield insight into
a perplexing fundamental question, namely why SMCs express multiple
alphaAR subtypes and how expression of the subtypes is regulated. The
findings could open up new opportunities in the study and understanding of
vascular hypertrophic diseases by establishing linkage among
catecholamines, ischemia, blood pressure and expression of specific
alphaAR subtypes that modulate SMC growth. In addition, these studies
will identify how intravascular pressure and tissue oxygen influence the
pattern and density of alpha-adrenergic receptor subtypes expressed by
vascular smooth muscle.
我们最近发现多达4种不同的肾上腺素受体
项目成果
期刊论文数量(7)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Oxygen modulates alpha 1B-adrenergic receptor gene expression by arterial but not venous vascular smooth muscle.
氧气通过动脉而非静脉血管平滑肌调节 α1B-肾上腺素能受体基因表达。
- DOI:10.1152/ajpheart.1996.271.4.h1599
- 发表时间:1996
- 期刊:
- 影响因子:0
- 作者:Eckhart,AD;Zhu,Z;Arendshorst,WJ;Faber,JE
- 通讯作者:Faber,JE
Platelet-derived growth factor-BB inhibits rat alpha1D-adrenergic receptor gene expression in vascular smooth muscle cells by inducing AP-2-like protein binding to alpha1D proximal promoter region.
血小板源性生长因子-BB 通过诱导 AP-2 样蛋白与 α1D 近端启动子区域结合,抑制大鼠血管平滑肌细胞中的 α1D 肾上腺素受体基因表达。
- DOI:10.1124/mol.56.6.1152
- 发表时间:1999
- 期刊:
- 影响因子:3.6
- 作者:Xin,X;Yang,N;Faber,JE
- 通讯作者:Faber,JE
CRE-like response element regulates expression of rat alpha 2D-adrenergic receptor gene in vascular smooth muscle.
CRE 样反应元件调节血管平滑肌中大鼠 α 2D 肾上腺素能受体基因的表达。
- DOI:10.1152/ajpheart.1997.273.1.h85
- 发表时间:1997
- 期刊:
- 影响因子:0
- 作者:Yang,N;Eckhart,AD;Xin,X;Faber,JE
- 通讯作者:Faber,JE
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JAMES E FABER其他文献
JAMES E FABER的其他文献
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{{ truncateString('JAMES E FABER', 18)}}的其他基金
Targeting the Pial Collateral Circulation for Mitigation of Cerebral Ischemia
针对软脑膜侧支循环缓解脑缺血
- 批准号:
9896889 - 财政年份:2013
- 资助金额:
$ 23.02万 - 项目类别:
Targeting the Pial Collateral Circulation for Mitigation of Cerebral Ischemia
针对软脑膜侧支循环缓解脑缺血
- 批准号:
8662826 - 财政年份:2013
- 资助金额:
$ 23.02万 - 项目类别:
Targeting the Pial Collateral Circulation for Mitigation of Cerebral Ischemia
针对软脑膜侧支循环缓解脑缺血
- 批准号:
8558449 - 财政年份:2013
- 资助金额:
$ 23.02万 - 项目类别:
Maintenance and Rarefaction of the Native Collateral Circulation
原生侧支循环的维持和稀疏
- 批准号:
8551687 - 财政年份:2012
- 资助金额:
$ 23.02万 - 项目类别:
Maintenance and Rarefaction of the Native Collateral Circulation
原生侧支循环的维持和稀疏
- 批准号:
8699824 - 财政年份:2012
- 资助金额:
$ 23.02万 - 项目类别:
Maintenance and Rarefaction of the Native Collateral Circulation
原生侧支循环的维持和稀疏
- 批准号:
8876770 - 财政年份:2012
- 资助金额:
$ 23.02万 - 项目类别:
Maintenance and Rarefaction of the Native Collateral Circulation
原生侧支循环的维持和稀疏
- 批准号:
8366973 - 财政年份:2012
- 资助金额:
$ 23.02万 - 项目类别:
Mechanisms of Collateral Development and Collateral Growth in Ischemia
缺血时的侧枝发育和侧枝生长机制
- 批准号:
7910685 - 财政年份:2008
- 资助金额:
$ 23.02万 - 项目类别:
Mechanisms of Collateral Development and Collateral Growth in Ischemia
缺血时的侧枝发育和侧枝生长机制
- 批准号:
7655324 - 财政年份:2008
- 资助金额:
$ 23.02万 - 项目类别:
Mechanisms of Collateral Development and Collateral Growth in Ischemia
缺血时的侧枝发育和侧枝生长机制
- 批准号:
8130993 - 财政年份:2008
- 资助金额:
$ 23.02万 - 项目类别:
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- 批准号:
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Central and renal alpha-adrenergic receptor with the development of salt-induced hypertension in Dahl-Iwai salt-sensitive rats.
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- 批准号:
03670461 - 财政年份:1991
- 资助金额:
$ 23.02万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
IDENTIFICATION AND FUNCTION OF ALPHA-ADRENERGIC RECEPTOR
α-肾上腺素能受体的鉴定和功能
- 批准号:
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