TRANSCRIPTIONAL CONTROL OF CARDIAC GROWTH

心脏生长的转录控制

• 批准号: 7720837
• 负责人: Kyu-Ho Lee
• 金额: $ 20.32万
• 依托单位: MEDICAL UNIVERSITY OF SOUTH CAROLINA
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-07-01 至 2009-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7720837
• 关键词: Affect; Anatomy; Aorta; Arteries; Biological Markers; Cardiac; Computer Retrieval of Information on Scientific Projects Database; Coronary artery; Defect; Development; Enhancers; Event; Funding; Grant; Growth; Heart; Institution; Mesoderm; Modeling; Mus; Myocardial; Neural Crest; Newborn Infant; Nucleic Acid Regulatory Sequences; Pattern; Population; Pulmonary artery structure; Regulation; Research; Research Personnel; Resources; Rotation; Signal Transduction; Source; Transcriptional Regulation; Transgenes; Transgenic Organisms; United States National Institutes of Health; congenital heart disorder; critical developmental period; mouse model; promoter

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. Congenital heart disease affects 0.5% of newborns each year, and approximately 20% of these defects are outflow tract (OFT) defects affecting proper formation of the great arteries of the heart, the aorta and the pulmonary artery. There are several models in mouse of congenital heart disease. However, these models provide an incomplete understanding of pathological events because few molecular markers sufficiently detail OFT anatomy during development and bifurcation into distinct vessels. In our studies of Nkx2.5 promoter regulation we have characterized a transgene that has asymmetric expression in the outflow tract during critical periods of outflow tract formation, expansion and septation. We plan to use these regulatory regions to analyze the relationship of early heart field and splanchnic mesoderm populations through development to formation of the mature great arteries during development. We plan to use this transgenic marker to examine OFT patterning and rotation events in several mouse models of OFT dysgenesis affecting myocardial, endocardial and cardiac neural crest populations. Also, through an analysis of the enhancer regions regulating asymmetric OFT and selective pulmonary artery versus aortic expression, we wish to understand the transcriptional factors and related signaling controlling great artery differentiation and underlying this important form of congenital heart disease.

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。 先天性心脏病每年影响0.5％的新生儿，其中约20％的缺陷是流出区（通常）缺陷，影响了心脏，主动脉和肺动脉的正确形成的正确形成。先天性心脏病小鼠中有几种模型。但是，这些模型对病理事件的理解提供了不完全的理解，因为在发育和分叉成分分为不同血管的过程中，很少有分子标记足够细节。在我们对NKX2.5启动子调节的研究中，我们表征了一个转基因，该转基因在流出道，扩张和分离的关键时期内在流出道中具有不对称表达。 我们计划使用这些调节区域来分析早期心脏领域和中胚层中胚层人群的关系，通过发展与发展过程中成熟大动脉的形成。 我们计划使用这种转基因标记来检查几种经常会影响心肌，心内和心脏神经crest群体的小鼠模型中的模式和旋转事件。 同样，通过对调节不对称OFT和选择性肺动脉与主动脉表达的增强剂区域的分析，我们希望理解控制大动脉分化的转录因子和相关信号传导，并为这种重要形式的先天性心脏病的形式提供了基础。