CAN CD 133 CELLS PREVENT HYPOXIA DRIVEN RETINAL NEOVASCULARISATION IN A RODENT MO
CAN CD 133 CELLS PREVENT HYPOXIA DRIVEN RETINAL NEOVASCULARISATION IN A RODENT MO
批准号:
7405687
负责人:
BELA ANAND-APTE
金额:
$31.06万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2007
资助国家:
美国
项目状态:
已结题
起止时间:
2007-09-30 至 2009-03-29
关键词:
Angiogenesis InhibitionAngiogenesis InhibitorsBlindnessBlood VesselsBusinessesCellsCentral VeinChoroidal NeovascularizationDevelopmentDiabetic RetinopathyDiseaseEventHematopoietic stem cellsHumanHyperoxiaHypoxiaInner Limiting MembraneIschemiaLeadLong-Term EffectsMarketingModelingMusNumbersPathologic NeovascularizationPatientsPharmaceutical PreparationsPhasePlayProliferatingResearchRetinalRetinal DiseasesRetinal NeovascularizationRetinal Vein OcclusionRetinopathy of PrematurityRodentRodent ModelRoleStem cellsTechnologyTestingTherapeuticTransplantationUmbilical cord structureVascularizationangiogenesisbasecell typeclinically significantneovascularneovascularizationnew technologynovel therapeuticsocular angiogenesisolder patientpreventproliferative diabetic retinopathyrepairedretina blood vessel structuretherapeutic angiogenesisvein occlusion
中文摘要
描述(申请人提供):眼血管生成的临床意义是巨大的,因为在西半球,糖尿病视网膜病变引起的视网膜新生血管是年轻患者新盲的最常见原因,而AMD导致的脉络膜新生血管(CNV)是导致老年患者严重且不可逆转的视力丧失的主要原因。在过去的几年里,血管生成的研究领域取得了很大的进展,这是因为有假设认为,抑制血管生成将是一种有用的策略,在许多眼部疾病中,病理性血管生成发挥了作用。视网膜新生血管涉及视网膜血管的萌芽,通常穿透内界膜(ILM)并生长到玻璃体。视网膜新生血管可见于糖尿病视网膜病变、早产儿视网膜病变、中心静脉阻塞和视网膜分支静脉阻塞等缺血性视网膜病变。抑制血管增殖是当前市场技术所采用的策略,并导致了大量试图靶向新生血管的药物的存在。即使这些药物在短期内在抑制眼部血管生成方面取得了一定的成功,并带来了症状的缓解,但作为初始原因的潜在血管丢失仍然没有得到治疗。此外,抗血管生成药物的长期效果尚不清楚。然而,可以假设它们可能导致血管丢失的加剧,这是新血管形成的诱因事件。治疗性干细胞是一项正在开发的相关新技术,目的是克服目前几种技术的缺点。在视网膜新生血管的小鼠模型中,造血干细胞已被证明可以挽救异常的视网膜血管。Artericell的核心业务集中于开发用于治疗性血管生成应用的“现成”干细胞产品。在这项研究中,该公司建议探索CD133血管母细胞作为一种细胞类型的特定用途,以挽救视网膜血管闭塞并减少糖尿病视网膜病变的新生血管效应。
英文摘要
DESCRIPTION (provided by applicant): The clinical significance of ocular angiogenesis is enormous, due to the fact that in the western hemisphere, retinal neovascularization resulting from diabetic retinopathy is the most common cause of new blindness in young patients, and choroidal neovascularization (CNV) resulting from AMD is the chief cause of severe and irreversible loss of vision in elderly patients. Over the past several years, much progress has been made in the field of angiogenesis research, fueled by the hypothesis that inhibition of angiogenesis would be a useful strategy to a number of ocular diseases in which pathologic angiogenesis plays a role. Retinal neovascularization involves the development of sprouts from retinal vessels, which usually penetrates the inner limiting membrane (ILM) and grows into the vitreous. Retinal neovascularization is observed in ischemic retinopathies such as diabetic retinopathy, retinopathy of prematurity, central vein occlusion and branch retinal vein occlusion. The inhibition of vessel proliferation is the strategy utilized by current market technologies and has led to the presence of a plethora of drugs attempting to target neovascularization. Even if the efforts of these drugs become somewhat successful in inhibiting ocular angiogenesis for the short term and bring symptomatic relief, the underlying vascular loss that is the initiating cause remains untreated. In addition the long-term effects of anti-angiogenic drugs are unclear. It can be assumed however that they might lead to the exacerbation of vessel loss, the precipitating event for neovascularization. Therapeutic stem cells is a relevant new technology being developed to overcome the shortcomings of several current technologies. Hematopoietic stem cells have been shown to rescue abnormal retinal vascularization in a murine model of retinal neovascularization. Arteriocyte's core business is focused on developing `off-the shelf' stem cell-based products for therapeutic angiogenesis applications. In this study the company proposes to explore the specific use of CD 133 hemangioblast as a cell type to rescue retinal vessel obliteration and diminish the neovascular effects of diabetic retinopathy.
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