DIVA-II

歌姬-II

• 批准号: 8173621
• 负责人: PRISCILLA E PEMU
• 金额: $ 12.9万
• 依托单位: MOREHOUSE SCHOOL OF MEDICINE
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-07-01 至 2011-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8173621
• 关键词: Antioxidants; Blood Vessels; Cells; Computer Retrieval of Information on Scientific Projects Database; Funding; Gene Expression; Gene Expression Profile; Genes; Grant; Institution; Insulin; Insulin Resistance; Lead; Maintenance; Mediating; NADPH Oxidase; Non obese; Obesity; Oxidative Stress; Research; Research Personnel; Resources; Source; Stem cells; Sympathetic Nervous System; United States National Institutes of Health; Up-Regulation; Women' s Group; copper zinc superoxide dismutase; exhaustion; human NOS3 protein; indexing; repaired; response

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Aim 1 Define the gene expression profile of endothelial progenitor cells of obese insulin resistant compared with obese non-insulin resistant and lean AA womenDefine expression of genes related to oxidative stress such as NADPH oxidase, endothelial nitric oxide synthase and copper zinc superoxide dismutase Define expression of genes related to insulin action and sympathetic nervous system activation Determine the relationship between antioxidant gene expression in EPCs among the three groups and levels of oxidative stress Hypothesis1: We hypothesize that the relationship between vascular stiffness (augmentation index) and the number of circulating endothelial progenitor cells shown in our earlier studies, is partly mediated through oxidative stress with up regulation of genes modulating oxidative stress. We anticipate that persistent oxidative stress will lead to exhaustion of the antioxidant mechanisms within the EPCs which will eventually impair the ability of these cells to assist in endothelial repair and maintenance of endothelial function. Furthermore, we hypothesize that there will be a difference in the gene expression profile among the three groups of women as a result of the response to oxidative stress

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 AIM 1与肥胖的非胰岛素耐药蛋白和瘦AA aa女性表达与氧化应激相关的基因表达相比，定义了肥胖胰岛素耐药性的内皮祖细胞的基因表达谱，例如NADPH氧化酶，例如内皮氧化物氧化物合成酶和铜锌氧化二氧化碳超氧化物雾化酶， 定义与胰岛素作用和交感神经系统激活有关的基因的表达 确定这三组和氧化应激水平之间EPC中抗氧化基因表达之间的关系 假设1：我们假设血管刚度（增强指数）与我们早期研究中所示的循环内皮祖细胞的数量之间的关系是通过氧化应激部分介导的，并加强调节氧化应激的基因。我们预计，持续的氧化应激将导致EPC中的抗氧化剂机制耗尽，这最终将损害这些细胞有助于内皮修复和维持内皮功能的能力。此外，我们假设三组女性在氧化应激的反应中，基因表达谱将有所不同。