Src Regulation of Lung Endothelial Barrier Function

Src 对肺内皮屏障功能的调节

基本信息

  • 批准号:
    8059132
  • 负责人:
  • 金额:
    $ 33.47万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2011
  • 资助国家:
    美国
  • 起止时间:
    2011-03-01 至 2016-02-29
  • 项目状态:
    已结题

项目摘要

In Project 4, we will test the hypotheses that (i) Nox2-dependent oxidant signaling activates Src kinasedependent ICAM-1-phosphorylation and thereby the recruitment of PMNs in the pulmonary circulation, and that (ii) Src phosphorylation of ICAM-1 in turn protracts Src activation and phosphorylation of caveolin-1 and dynamin-2, thereby triggering caveolae-mediated transcytosis of albumin and endothelial hyper-permeability. These studies will address the following Specific Aims: (1) role of PI3-kinase, PKC zeta, Nox2, and Src signaling, and of Akt phosphorylation of filamin A in the mechanism of ICAM-1 phosphorylation, clustering, and rapid increase in ICAM-1 binding affinity in lung microvascular endothelial cells and PMN uptake in lungs; (2) role of phospho-ICAM-1 in recruitment of SHP2 and protracting Src activation and thereby caveolin-1 and dynamin-2 activation, and thus stimulating caveolae-mediated transcytosis and hyper-permeability of albumin. Project 4 will delineate the signaling mechanisms mediating the post-translafional modification of ICAM-1 in pulmonary microvessel endothelial cells using imaging, cell biology, biochemical, and physiological approaches. We will thereby establish how endothelial cell ICAM-1 shifts to a high-affinity state and promotes PMN adhesion and sequestration and also induces caveolae-mediated hyper-permeability via the transcytosis of albumin. These studies it is hoped will lead to a new understanding of the early PMN-mediated lung inflammatory response and its coupling to lung vascular hyper-permeability. Identification of the key signaling hubs of ICAM-1-mediated endothelial adhesivity and activation of the caveolae-mediated albumin transport pathway is likely to provide novel therapeutic targets directed against infiammatory lung injury.
在项目4中,我们将测试(i) nox2依赖的氧化信号激活Src激酶依赖的假设

项目成果

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RICHARD D MINSHALL其他文献

RICHARD D MINSHALL的其他文献

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{{ truncateString('RICHARD D MINSHALL', 18)}}的其他基金

Fibroblast Mediated Mechanisms of Pulmonary Hypertension
成纤维细胞介导的肺动脉高压机制
  • 批准号:
    10163897
  • 财政年份:
    2019
  • 资助金额:
    $ 33.47万
  • 项目类别:
Fibroblast Mediated Mechanisms of Pulmonary Hypertension
成纤维细胞介导的肺动脉高压机制
  • 批准号:
    10378641
  • 财政年份:
    2019
  • 资助金额:
    $ 33.47万
  • 项目类别:
Fibroblast Mediated Mechanisms of Pulmonary Hypertension
成纤维细胞介导的肺动脉高压机制
  • 批准号:
    10599245
  • 财政年份:
    2019
  • 资助金额:
    $ 33.47万
  • 项目类别:
Fibroblast Mediated Mechanisms of Pulmonary Hypertension
成纤维细胞介导的肺动脉高压机制
  • 批准号:
    9912845
  • 财政年份:
    2019
  • 资助金额:
    $ 33.47万
  • 项目类别:
Imaging and Physiology Core
影像和生理学核心
  • 批准号:
    8059138
  • 财政年份:
    2011
  • 资助金额:
    $ 33.47万
  • 项目类别:
Caveolin-1 and NO Regulate PMN-mediated Increases in Vascular Permeability
Caveolin-1 和 NO 调节 PMN 介导的血管通透性增加
  • 批准号:
    7822536
  • 财政年份:
    2009
  • 资助金额:
    $ 33.47万
  • 项目类别:
CORE--Imaging and Physiology Core
CORE--影像与生理学核心
  • 批准号:
    7367826
  • 财政年份:
    2007
  • 资助金额:
    $ 33.47万
  • 项目类别:
Zeiss Dynamic Laser TIRF
蔡司动态激光 TIRF
  • 批准号:
    7217104
  • 财政年份:
    2007
  • 资助金额:
    $ 33.47万
  • 项目类别:
Src Regulation of Lung Endothelial Barrier Function
Src 对肺内皮屏障功能的调节
  • 批准号:
    7367823
  • 财政年份:
    2007
  • 资助金额:
    $ 33.47万
  • 项目类别:
Src Regulation of Lung Endothelial Barrier Function
Src 对肺内皮屏障功能的调节
  • 批准号:
    7312502
  • 财政年份:
    2006
  • 资助金额:
    $ 33.47万
  • 项目类别:

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