PROTEIN KINASE C & CELL CYCLE IN VASCULAR INJURY
蛋白激酶C
基本信息
- 批准号:2750461
- 负责人:
- 金额:$ 10.78万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:1996
- 资助国家:美国
- 起止时间:1996-08-01 至 2000-07-31
- 项目状态:已结题
- 来源:
- 关键词:DNA replication aorta biological signal transduction blood vessel disorder calcium channel calcium channel blockers cell cycle cell growth regulation diacylglycerols enzyme activity gel electrophoresis immunoprecipitation injury inositol phosphates isozymes laboratory rat northern blottings protein kinase C regulatory gene tissue /cell culture vascular smooth muscle western blottings
项目摘要
DESCRIPTION (Adapted from Investigator's Abstract): This application
for a FIRST Award examines the role of activation of protein kinase C in
immediate early gene expression following balloon catheter-induced injury
of the rat thoracic aorta (BAL). Enhanced smooth muscle cell (SMC)
proliferation and migration account for the intimal thickening which
results from BAL of the rat thoracic aorta. The imposition of stretch
upon SMC is inevitable in BAL, which produces a greater SMC
proliferative response as compared to endothelial denudation alone.
Protein kinase C (PKC) inhibitors and calcium channel blockers are known
to modulate SMC proliferation in vitro, and the latter compounds reduce
proliferation following BAL in vivo. The fundamental goal of this
application is to delineate early calcium dependent signal transduction
mechanisms responsible for stretch-induced activation of quiescent SMC
in vivo, which in association with humoral factors, results in
activation of the SMC cell cycle. The first two Aims center upon BAL
stretch-induced regulation of PKC in an in situ perfused aortic
preparation. Aim 1 covers the time course and calcium dependence for
stretch-induced activation and membrane translocation of both the
calcium sensitive and insensitive PKC isoforms. Aim 2 characterizes the
time course and requirements for biphasic generation of the PKC cofactor
diacylglycerol and inositol 3,4,5-trisphosphate. These findings will
be extended using SMC in vitro in Aim 3. This Aim will examine
translocation and down regulation of specific PKCs during the G1 phase
of the cell cycle in vitro. The SMC in the vessel wall possesses a
"contractile" phenotype whose growth is inhibited by heparinoid
molecules associated with the extracellular matrix. Compared to
proliferating "synthetic" SMC in vitro, the perfusion model is more
relevant in that stretch-related signal transduction mechanisms in situ
are more likely to mimic the earliest activation response of quiescent
SMC in vivo. It is recognized the PKC and cell cycle studies in the in
vitro system reflects growth control in cells that are persistently
proliferative and in which the modeling of stretch may be limited.
However, these studies serve as a basis of subsequent investigation of
the role of PKC on the regulation of the cell cycle in differentiated
vessel wall SMC.
描述(改编自研究者摘要):本应用
项目成果
期刊论文数量(0)
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CAROLYN J SMITH其他文献
CAROLYN J SMITH的其他文献
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{{ truncateString('CAROLYN J SMITH', 18)}}的其他基金
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