Anti-Angiogenic Preeclamptic Milieu Impairs Infant Lung and Vascular Development

抗血管生成先兆子痫环境损害婴儿肺和血管发育

基本信息

项目摘要

DESCRIPTION (provided by applicant): Preeclampsia, which is characterized by maternal hypertension and systemic endothelial vascular dysfunction, occurs in 3-8% of pregnancies and is associated with significant neonatal morbidities. Among infants born premature, preeclampsia is independently associated with a high risk of bronchopulmonary dysplasia (BPD), as well as an increased risk of other systemic complications. Even late preterm infants born to preeclamptic women have higher respiratory morbidity, greater rates of respiratory distress syndrome, increased rates of NICU admission, longer neonatal hospitalization, and increased respiratory support needs compared to normotensive pregnancies. The pathogenesis of preeclampsia relates to overproduction of soluble vascular endothelial growth factor (VEGF) receptor-1 (sFlt-1), which inhibits VEGF signaling. The excess sFlt-1 in maternal serum, as well as in amniotic fluid, correlates with the severity of preeclampsia. In addition, neonatal cord bloo from pregnancies complicated by preeclampsia has increased sFlt-1, reduced VEGF levels, and decreased numbers and function of angiogenic circulating progenitor cells (CPCs). Therefore, the anti-angiogenic environment of preeclampsia likely impairs angiogenic processes in the fetus and infant. We hypothesize that the anti-angiogenic environment in pregnant mothers with preeclampsia impairs pulmonary and vascular development in the infant. The overall objective of our study will be achieved in the following Specific Aims: SA #1: A) Determine whether preeclampsia impairs infant lung development, as evidenced by reduced pulmonary diffusion capacity and airway function. B) Examine whether impaired lung function is related to the angiogenic environment in cord blood, as evidenced by fewer CPCs, decreased CPC: nonCPC ratio, reduced VEGF, and increased sFlt-1. SA #2: A) Determine whether preeclampsia impairs infant systemic vascular function, as evidenced by reduced capillary density, increased vasoreactivity, and increased blood pressure. B) Examine whether impaired systemic vascular function is related to the angiogenic environment in cord blood, as evidenced by fewer CPCs, reduced CPC: nonCPC ratio, reduced VEGF, and increased sFlt-1.
描述(由申请人提供):先兆子痫的特征是母体高血压和全身性内皮血管功能障碍,发生在3-8%的妊娠中,并与明显的新生儿病态有关。在出生的早产婴儿中,先兆子痫与支气管肺发育不良(BPD)的高风险以及其他全身并发症的风险增加。与正常怀孕相比,即使是先兆子痫妇女出生的早期婴儿的呼吸发病率更高,呼吸窘迫综合征的发生率更高,入院率提高,新生儿住院时间更长以及与正常性怀孕相比,呼吸支持需求增加。先兆子痫的发病机理与可溶性血管内皮生长因子(VEGF)受体1(SFLT-1)的生产过多有关,该因子抑制了VEGF信号传导。母体血清以及羊水中的过量SFLT-1与先兆子痫的严重程度有关。此外,先兆子痫的怀孕复杂性的新生儿绳索增加了SFLT-1,VEGF水平降低,血管生成循环祖细胞(CPC)的数量和功能降低。因此,先兆子痫的抗血管生成环境可能会损害胎儿和婴儿中的血管生成过程。我们假设先兆子痫的怀孕母亲的抗血管生成环境会损害婴儿的肺部和血管发育。我们研究的总体目标将在以下特定目的中实现:SA#1:a)确定先兆子痫是否会损害婴儿肺发育,这可以通过降低的肺扩散能力和气道功能证明。 b)检查肺功能受损是否与脐带血的血管生成环境有关,如CPC较少,CPC:非CPC比率降低,VEGF降低和SFLT-1增加。 SA#2:a)确定先兆子痫是否会损害婴儿的全身血管功能,这是毛细血管密度降低,血管反应性升高和血压升高所证明的。 b)检查系统性血管功能受损是否与脐带血的血管生成环境有关,这一点有CPC的较少,CPC降低:非CPC比率,降低VEGF和SFLT-1的增加。

项目成果

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Laura S Haneline其他文献

Laura S Haneline的其他文献

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{{ truncateString('Laura S Haneline', 18)}}的其他基金

Anti-Angiogenic Preeclamptic Milieu Impairs Infant Lung and Vascular Development
抗血管生成先兆子痫环境损害婴儿肺和血管发育
  • 批准号:
    8814313
  • 财政年份:
    2015
  • 资助金额:
    $ 64.81万
  • 项目类别:
Anti-Angiogenic Preeclamptic Milieu Impairs Infant Lung and Vascular Development
抗血管生成先兆子痫环境损害婴儿肺和血管发育
  • 批准号:
    9274355
  • 财政年份:
    2015
  • 资助金额:
    $ 64.81万
  • 项目类别:
Circulating Endothelial Progenitor Cell Subsets
循环内皮祖细胞亚群
  • 批准号:
    8261209
  • 财政年份:
    2011
  • 资助金额:
    $ 64.81万
  • 项目类别:
Endothelial Progenitor and Vascular Dysfunction in Infants of Diabetic Mothers
糖尿病母亲的婴儿的内皮祖细胞和血管功能障碍
  • 批准号:
    8307245
  • 财政年份:
    2009
  • 资助金额:
    $ 64.81万
  • 项目类别:
Endothelial Progenitor and Vascular Dysfunction in Infants of Diabetic Mothers
糖尿病母亲的婴儿的内皮祖细胞和血管功能障碍
  • 批准号:
    7730571
  • 财政年份:
    2009
  • 资助金额:
    $ 64.81万
  • 项目类别:
Endothelial Progenitor and Vascular Dysfunction in Infants of Diabetic Mothers
糖尿病母亲的婴儿的内皮祖细胞和血管功能障碍
  • 批准号:
    7901560
  • 财政年份:
    2009
  • 资助金额:
    $ 64.81万
  • 项目类别:
Endothelial Progenitor and Vascular Dysfunction in Infants of Diabetic Mothers
糖尿病母亲的婴儿的内皮祖细胞和血管功能障碍
  • 批准号:
    8081016
  • 财政年份:
    2009
  • 资助金额:
    $ 64.81万
  • 项目类别:
GDM Effect on Maternal and Neonatal Endothelial Progenitors and Vascular Function
GDM 对孕产妇和新生儿内皮祖细胞和血管功能的影响
  • 批准号:
    7295819
  • 财政年份:
    2006
  • 资助金额:
    $ 64.81万
  • 项目类别:
GDM Effect on Maternal/Neonatal Endothelial Progenitors
GDM 对母体/新生儿内皮祖细胞的影响
  • 批准号:
    7233320
  • 财政年份:
    2006
  • 资助金额:
    $ 64.81万
  • 项目类别:
Role of ASK1 and PKR in Fancc hematopoiesis
ASK1 和 PKR 在 Fancc 造血中的作用
  • 批准号:
    6918154
  • 财政年份:
    2005
  • 资助金额:
    $ 64.81万
  • 项目类别:

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