Harnessing blood clot clearance mechanisms after germinal matrix hemorrhage

利用生发基质出血后的血凝块清除机制

基本信息

  • 批准号:
    10331887
  • 负责人:
  • 金额:
    $ 39.5万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2021
  • 资助国家:
    美国
  • 起止时间:
    2021-02-01 至 2025-11-30
  • 项目状态:
    未结题

项目摘要

Abstract Germinal matrix hemorrhage (GMH) is one of the leading causes of morbidity, mortality, and acquired infantile hydrocephalus in preterm infants in the United States, with little progress made in its clinical management. Blood clots have been shown to elicit secondary brain injury after GMH, by disrupting normal cerebrospinal fluid circulation and absorption after germinal matrix hemorrhage causing post-hemorrhagic hydrocephalus development. Current experimental evidence suggests that rapid hematoma resolution is necessary to quickly ameliorate inflammation and improve neurological outcomes after hemorrhagic stroke. N-formyl peptide receptor 2 (FPR2), a G-protein-coupled receptor, has been shown to be neuroprotective after stroke. FPR2 activation has been associated with the upregulation of phagocytic macrophage clearance, yet its mechanism has not been fully explored. Recent literature suggests that FPR2 may play a role in the stimulation of scavenger receptor CD36. Scavenger receptor CD36, a trans-membrane glycoprotein, plays a vital role in microglia phagocytic blood clot clearance after GMH. FPR2 has been shown to activate extracellular-signal-regulated kinase 1/2 (ERK1/2), which promotes the transcription of the dual-specificity protein phosphatase 1 (DUSP1) gene. Current literature suggests that DUSP1 may act on CD36 receptor and may play a role in FPR2 induced phagocytosis. Our preliminary suggests that FPR2 activation enhances hematoma resolution and improves neurological deficits. Therefore, we seek to elucidate the underlying hematoma resolving mechanism of FPR2. We hypothesize that FPR2 stimulation enhances microglia induced hematoma resolution through the activation of the ERK (1/2)/DUSP1/CD36 signaling pathway, thereby improving short- and long-term neurological outcomes. Aim 1 will investigate the role of FPR2 in enhancing hematoma resolution, thereby improving neurological function following GMH. Aim 2 will investigate FPR2-induced activation of the ERK/DUSP1/CD36 signaling pathway after GMH. The long-term goal of this proposal is to provide a basis for clinical translation of FPR2 stimulation as an effective non-invasive therapeutic strategy to protect against acute and chronic complications in the GMH patient population.
摘要

项目成果

期刊论文数量(0)
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会议论文数量(0)
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Jiping Tang其他文献

Jiping Tang的其他文献

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{{ truncateString('Jiping Tang', 18)}}的其他基金

Harnessing blood clot clearance mechanisms after germinal matrix hemorrhage
利用生发基质出血后的血凝块清除机制
  • 批准号:
    10528489
  • 财政年份:
    2021
  • 资助金额:
    $ 39.5万
  • 项目类别:
Harnessing blood clot clearance mechanisms after germinal matrix hemorrhage
利用生发基质出血后的血凝块清除机制
  • 批准号:
    10203222
  • 财政年份:
    2021
  • 资助金额:
    $ 39.5万
  • 项目类别:
Investigating the role of mast cells in neonatal germinal matrix hemorrhage
研究肥大细胞在新生儿生发基质出血中的作用
  • 批准号:
    9452501
  • 财政年份:
    2017
  • 资助金额:
    $ 39.5万
  • 项目类别:
Mechanisms of G-CSF-Induced Neuroprotection
G-CSF 诱导的神经保护机制
  • 批准号:
    8112459
  • 财政年份:
    2009
  • 资助金额:
    $ 39.5万
  • 项目类别:
Mechanisms of G-CSF-Induced Neuroprotection
G-CSF 诱导的神经保护机制
  • 批准号:
    7725844
  • 财政年份:
    2009
  • 资助金额:
    $ 39.5万
  • 项目类别:
Mechanisms of G-CSF-Induced Neuroprotection
G-CSF 诱导的神经保护机制
  • 批准号:
    8288863
  • 财政年份:
    2009
  • 资助金额:
    $ 39.5万
  • 项目类别:
Mechanisms of G-CSF-Induced Neuroprotection
G-CSF 诱导的神经保护机制
  • 批准号:
    7905765
  • 财政年份:
    2009
  • 资助金额:
    $ 39.5万
  • 项目类别:
Role of NADPH Oxidase in ICH-Induced Brain Injury
NADPH 氧化酶在 ICH 引起的脑损伤中的作用
  • 批准号:
    6958794
  • 财政年份:
    2005
  • 资助金额:
    $ 39.5万
  • 项目类别:
Role of NADPH Oxidase in ICH-Induced Brain Injury
NADPH 氧化酶在 ICH 引起的脑损伤中的作用
  • 批准号:
    7140282
  • 财政年份:
    2005
  • 资助金额:
    $ 39.5万
  • 项目类别:
Gleevec Protects Neurovascular Unit by Inhibition of PDGFR
格列卫通过抑制 PDGFR 保护神经血管单位
  • 批准号:
    8993927
  • 财政年份:
  • 资助金额:
    $ 39.5万
  • 项目类别:

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