Reciprocal VEGFC/VEGFR3-CDH5 regulation of lymphatic and sinusoidal vascular growth
VEGFC/VEGFR3-CDH5 对淋巴管和窦状血管生长的相互调节
基本信息
- 批准号:10608143
- 负责人:
- 金额:$ 60.63万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2022
- 资助国家:美国
- 起止时间:2022-05-01 至 2026-04-30
- 项目状态:未结题
- 来源:
- 关键词:AccelerationAnemiaAnimalsBlood VesselsBone MarrowBone Marrow TransplantationC cadherinCadherinsCell ProliferationCytoskeletonDefectDiseaseEdemaEndocytosisEndosomesEndothelial CellsEndotheliumErythroidExhibitsFetal LiverGeneticGenetic studyGrowthHematopoiesisHematopoieticHepatocyteIn VitroKDR geneLymphLymphangiogenesisLymphaticLymphatic CapillariesLymphatic Endothelial CellsLymphedemaMarrowMediatingMolecularMusNatural regenerationOrganPathway interactionsPatientsPermeabilityPhenocopyPhenotypePhosphorylationPregnancyRecoveryRegulationRegulatory PathwayRoleSignal TransductionTailTestingTranslationsTyrosineVEGFA geneVEGFC geneVascular DiseasesVascular Endothelial Growth Factor CVascular Endothelial Growth Factor Receptor-3Vascular Endothelial Growth Factorsbone cellcadherin 5cell motilityfetalgain of functionimprovedin vivoinsightirradiationloss of functionlymphatic developmentlymphatic vesselmature animalnovel therapeutic interventiontraffickingtranslational impactvascular bed
项目摘要
Project Summary
Sinusoidal and lymphatic vessel regeneration are predicted to improve treatment of
hematopoietic diseases and lymphedema, but are presently limited by an incomplete
understanding of the molecular and genetic pathways that control growth of these
specialized vascular beds. Prior studies by us and others have demonstrated that
VEGFC is required for fetal liver hematopoiesis, but a clear mechanism for this
requirement has not been identified. Our preliminary studies demonstrate that loss of
VEGFC/VEGFR3 function or gain of CDH5 function confers identical defects in
sinusoidal and lymphatic vascular growth. Further, our genetic studies demonstrate that
partial loss of CDH5 rescues both the anemia and edema conferred by the loss
sinusoidal and lymphatic vascular growth, respectively, in VEGFR3-deficient animals.
We hypothesize that a reciprocal VEGFC/VEGFR3-CDH5 regulatory loop controls
sinusoidal and lymphatic vascular growth. This proposal will test this hypothesis in vivo
and in vitro, investigate the molecular mechanism of this co-regulatory axis, and
determine whether manipulation of CDH5 can be used to stimulate sinusoidal and
lymphatic regeneration in mature animals. These studies are predicted to provide
fundamental new insights into sinusoidal and lymphatic vessel growth that may be
leveraged to treat patients with hematopoietic and lymphatic vascular diseases.
项目总结
项目成果
期刊论文数量(0)
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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MARK L KAHN其他文献
MARK L KAHN的其他文献
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{{ truncateString('MARK L KAHN', 18)}}的其他基金
Genetic Investigation of Covid 19 in Lung Disease
Covid 19 在肺部疾病中的基因研究
- 批准号:
10673004 - 财政年份:2022
- 资助金额:
$ 60.63万 - 项目类别:
Reciprocal VEGFC/VEGFR3-CDH5 regulation of lymphatic and sinusoidal vascular growth
VEGFC/VEGFR3-CDH5 对淋巴管和窦状血管生长的相互调节
- 批准号:
10417684 - 财政年份:2022
- 资助金额:
$ 60.63万 - 项目类别:
Genetic Investigation of Covid 19 in Lung Disease
Covid 19 在肺部疾病中的基因研究
- 批准号:
10502908 - 财政年份:2022
- 资助金额:
$ 60.63万 - 项目类别:
Genetic Investigation of Covid 19 in Lung Disease
Covid 19 在肺部疾病中的基因研究
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10768221 - 财政年份:2022
- 资助金额:
$ 60.63万 - 项目类别:
Molecular and genetic basis of deep venous thrombosis
深静脉血栓形成的分子和遗传学基础
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10460687 - 财政年份:2021
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Flow and endothelial signaling in acquired myxomatous valve disease
获得性粘液瘤性瓣膜疾病中的血流和内皮信号传导
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10226236 - 财政年份:2020
- 资助金额:
$ 60.63万 - 项目类别:
Flow and endothelial signaling in acquired myxomatous valve disease
获得性粘液瘤性瓣膜疾病中的血流和内皮信号传导
- 批准号:
10626893 - 财政年份:2020
- 资助金额:
$ 60.63万 - 项目类别:
Flow and endothelial signaling in acquired myxomatous valve disease
获得性粘液瘤性瓣膜疾病中的血流和内皮信号传导
- 批准号:
10033435 - 财政年份:2020
- 资助金额:
$ 60.63万 - 项目类别:
Flow and endothelial signaling in acquired myxomatous valve disease
获得性粘液瘤性瓣膜疾病中的血流和内皮信号传导
- 批准号:
10408810 - 财政年份:2020
- 资助金额:
$ 60.63万 - 项目类别:
MEKK3 signaling in hemogenic endothelium
造血内皮细胞中的 MEKK3 信号传导
- 批准号:
10198023 - 财政年份:2018
- 资助金额:
$ 60.63万 - 项目类别:
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