Non-Resident Lung angiogenic precursor cells in bronchopulmonary dysplasia
支气管肺发育不良中的非驻留肺血管生成前体细胞
基本信息
- 批准号:8237059
- 负责人:
- 金额:$ 36.77万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2008
- 资助国家:美国
- 起止时间:2008-04-01 至 2013-03-31
- 项目状态:已结题
- 来源:
- 关键词:AdolescenceAdultAdverse effectsAffectAlveolarAnimalsAsthmaBlood CirculationBlood VesselsBone MarrowBone Marrow CellsBronchopulmonary DysplasiaCD34 geneCardiovascular systemCell CountCell surfaceCellsChildChronic Obstructive Airway DiseaseChronic lung diseaseDataDevelopmentEndothelial CellsEngraftmentEnvironmental air flowEvolutionExerciseExposure toGasesGoalsGrowthGrowth and Development functionHealedHematopoieticHomingHyperoxiaIn VitroIncidenceInfantInjuryKidneyLeadLungMaintenanceModelingMusNeonatalNitric OxideOxygenPTPRC genePlayPopulationPremature BirthPremature InfantPulmonary CirculationPulmonary HypertensionPulmonary artery structureRattusRecoveryRodentRoleSecondary toSignal TransductionSiteSourceStem cellsStructureTechniquesTherapeuticTherapeutic InterventionVascular Endothelial Growth Factor ReceptorVascular Endothelial Growth Factor Receptor-2Vascular Endothelial Growth FactorsWorkantiangiogenesis therapybasecell growthcritical periodcytokinedensityemerging adulthealinghigh riskhuman NOS3 proteinimprovedinfancyinjuredlung developmentlung injurylung preservationlung repairmortalitymouse modelneonatal exposureneonatal lung injuryneonatenovelnovel therapeutic interventionoxygen toxicityprecursor cellreceptorresponse to injuryvasculogenesis
项目摘要
DESCRIPTION (provided by applicant): Bronchopulmonary dysplasia (BPD) is a chronic lung disease of infancy that is the result of premature birth. Infants with BPD have abnormal lung structure that is characterized by reduced pulmonary vascular density and a dysmorphic vascular structure. This results in impaired gas exchange, exercise intolerance, pulmonary hypertension, an increased incidence of asthma and early mortality. The mechanisms that impair lung development are poorly understood and there are few therapeutic interventions in the treatment of BPD. Recently, circulating angiogenic or endothelial progenitor cells (EPC) have been identified and characterized. These EPCs are believed to play a role in the recovery of blood vessels after injury. The role of EPCs during normal lung vascular and alveolar growth is unknown. In addition, the role these cells play in the neonate during the recovery from lung injury is unknown. Our goal is to characterize the role of EPCs in lung growth and development and determine if these cells are able to play a role in lung vascular and alveolar growth during and in recovery after lung injury. We propose the following hypothesis that a reduction in the mobilization, engraftment and survival of non- resident lung endothelial precursor cells (EPCs), is a mechanism contributing to impaired lung vascular and alveolar growth during and after exposure to neonatal hyperoxia. In order to study this hypothesis we are proposing the following specific aims in a mouse model: 1) To determine the therapeutic role of exogenous EPCs in the maintenance of lung vascular and alveolar growth during exposure to, and in the recovery from, neonatal moderate hyperoxia. 2) To determine if non-resident lung bone marrow derived cells participate in the preservation of lung structure during moderate hyperoxia exposure of adult mice. 3) To study, in vitro, the mechanisms by which VEGF, Epo, NO and hyperoxia affect EPC growth and function. PROJECT NARRATIVE: We expect that the results of this study will provide a better understanding of the roles and mechanisms by which extrinsic (circulating) cells and intrinsic (resident lung) cells play in lung vascular and alveolar growth, especially during and in the recovery from neonatal lung injury. A better understanding of these mechanisms of neonatal lung injury and repair may lead to novel therapies in the treatment of BPD.
描述(由申请人提供):支气管肺发育不良(BPD)是一种婴儿期慢性肺部疾病,是早产的结果。患有BPD的婴儿具有异常的肺结构,其特征在于肺血管密度降低和畸形的血管结构。这导致气体交换受损、运动不耐受、肺动脉高压、哮喘发病率增加和早期死亡。损害肺发育的机制知之甚少,BPD的治疗干预很少。最近,循环血管生成或内皮祖细胞(EPC)已被确定和表征。这些EPCs被认为在损伤后血管的恢复中发挥作用。EPCs在正常肺血管和肺泡生长中的作用尚不清楚。此外,这些细胞在新生儿肺损伤恢复过程中的作用尚不清楚。我们的目标是表征EPCs在肺生长和发育中的作用,并确定这些细胞是否能够在肺损伤期间和肺损伤后的恢复中在肺血管和肺泡生长中发挥作用。我们提出以下假设:非常驻肺内皮前体细胞(EPCs)的动员、植入和存活减少是导致新生儿高氧暴露期间和之后肺血管和肺泡生长受损的机制。为了研究这一假设,我们提出了以下具体目标,在小鼠模型:1)确定外源性EPCs的治疗作用,在维持肺血管和肺泡生长暴露期间,并在恢复,新生儿中度高氧。2)目的:探讨非驻留肺骨髓源性细胞是否参与成年小鼠中度高氧暴露时肺结构的保护。3)探讨血管内皮生长因子(VEGF)、促红细胞生成素(Epo)、一氧化氮(NO)和高氧对内皮祖细胞(EPC)生长和功能的影响。项目叙述:我们希望本研究的结果将提供一个更好的理解的作用和机制,其中外在(循环)细胞和内在(居民肺)细胞在肺血管和肺泡生长,特别是在新生儿肺损伤的恢复过程中发挥。更好地理解新生儿肺损伤和修复的这些机制可能会导致BPD治疗的新疗法。
项目成果
期刊论文数量(2)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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Vivek Balasubramaniam其他文献
Vivek Balasubramaniam的其他文献
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{{ truncateString('Vivek Balasubramaniam', 18)}}的其他基金
Non-Resident Lung angiogenic precursor cells in bronchopulmonary dysplasia
支气管肺发育不良中的非驻留肺血管生成前体细胞
- 批准号:
7591125 - 财政年份:2008
- 资助金额:
$ 36.77万 - 项目类别:
Non-Resident Lung angiogenic precursor cells in bronchopulmonary dysplasia
支气管肺发育不良中的非驻留肺血管生成前体细胞
- 批准号:
8040938 - 财政年份:2008
- 资助金额:
$ 36.77万 - 项目类别:
Non-Resident Lung angiogenic precursor cells in bronchopulmonary dysplasia
支气管肺发育不良中的非驻留肺血管生成前体细胞
- 批准号:
7463422 - 财政年份:2008
- 资助金额:
$ 36.77万 - 项目类别:
Non-Resident Lung angiogenic precursor cells in bronchopulmonary dysplasia
支气管肺发育不良中的非驻留肺血管生成前体细胞
- 批准号:
7789611 - 财政年份:2008
- 资助金额:
$ 36.77万 - 项目类别:
Endothelial Growth Factor&Nitric Oxide in Lung Vas.Dev
内皮生长因子
- 批准号:
6770062 - 财政年份:2003
- 资助金额:
$ 36.77万 - 项目类别:
VEGF and Nitric Oxide in Lung Vascular Development
肺血管发育中的 VEGF 和一氧化氮
- 批准号:
6670935 - 财政年份:2003
- 资助金额:
$ 36.77万 - 项目类别:
VEGF and Nitric Oxide in Lung Vascular Development
肺血管发育中的 VEGF 和一氧化氮
- 批准号:
7247192 - 财政年份:2003
- 资助金额:
$ 36.77万 - 项目类别:
Endothelial Growth Factor&Nitric Oxide in Lung Vas.Dev
内皮生长因子
- 批准号:
6917812 - 财政年份:2003
- 资助金额:
$ 36.77万 - 项目类别:
Endothelial Growth Factor&Nitric Oxide in Lung Vas.Dev
内皮生长因子
- 批准号:
7101109 - 财政年份:2003
- 资助金额:
$ 36.77万 - 项目类别:
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