Targeted Angiogenesis in a Three-Dimensional Scaffold.

三维支架中的靶向血管生成。

• 批准号: 7117745
• 负责人: Michael E Davis
• 金额: $ 5.04万
• 依托单位: EMORY UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2004
• 资助国家: 美国
• 起止时间: 2004-09-01 至 2007-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7117745
• 关键词: angiogenesis; bioengineering /biomedical engineering; biomaterial compatibility; biomaterial development /preparation; biotechnology; capillary; cardiac myocytes; cardiovascular disorder therapy; cell differentiation; cell growth regulation; cell proliferation; congestive heart failure; gel; implant; injection /infusion; laboratory mouse; medical implant science; molecular assembly /self assembly; newborn animals; peptides; postdoctoral investigator; tissue engineering; tissue support frame; vascular endothelial growth factors; vascular endothelium

DESCRIPTION (provided by applicant): Tissue engineering has become a promising and emerging area of research to treat a variety of physiological conditions ranging from orthopedic-related to cardiac-related problems. Congestive heart failure is a leading cause of morbidity and mortality in the United States and is increasing throughout the world. A major cause of heart failure is the loss and limited regeneration of cardiomyocytes. Therefore, tissue engineering of myocardium is an actively developing area of research to restore cardiac function. There have been several studies that have demonstrated successful engineering of functional myocardium. In this study, I propose exploring a new approach for in vivo engineering of cardiac tissue - to use a spontaneous vascularizing scaffold as a 3-dimensional substrate for cardiac tissue formation through testing of specific hypotheses. Specifically, Aim 1 will test the hypothesis that a self-assembling peptide gel promotes spontaneous angiogenesis in vivo, by endogenous endothelial cells. Aim 2 will test the hypothesis that targeting growth factors to the peptide gel will accelerate endothelial cell differentiation and capillary formation, resulting in improved survival of implanted cardiomyocytes.

描述（由申请人提供）：组织工程已成为一个有前景的新兴研究领域，用于治疗从骨科相关问题到心脏相关问题等各种生理状况。充血性心力衰竭是美国发病率和死亡率的主要原因，并且在世界各地正在增加。心力衰竭的一个主要原因是心肌细胞的损失和有限的再生。因此，心肌组织工程是恢复心脏功能的一个积极发展的研究领域。已有多项研究证明功能性心肌的工程化是成功的。在这项研究中，我建议探索一种心脏组织体内工程的新方法 - 通过测试特定假设，使用自发血管化支架作为心脏组织形成的 3 维基质。具体来说，目标 1 将测试自组装肽凝胶通过内源性内皮细胞促进体内自发血管生成的假设。目标 2 将检验以下假设：将生长因子靶向肽凝胶将加速内皮细胞分化和毛细血管形成，从而提高植入的心肌细胞的存活率。

项目成果

Endothelial-cardiomyocyte interactions in cardiac development and repair.

心脏发育和修复中的内皮-心肌细胞相互作用。

• DOI: 10.1146/annurev.physiol.68.040104.124629
• 发表时间: 2006-02-06
• 期刊: Annual review of physiology
• 作者: P. Hsieh;Michael E. Davis;Laura K Lisowski;Richard T. Lee
• 通讯作者: Richard T. Lee

Injectable self-assembling peptide nanofibers create intramyocardial microenvironments for endothelial cells.

可注射的自组装肽纳米纤维为内皮细胞创造心肌内微环境。

• 发表时间: 2005-02-01
• 影响因子: 37.8
• 作者: Davis, Michael E;Motion, J P Michael;Narmoneva, Daria A;Takahashi, Tomosaburo;Hakuno, Daihiko;Kamm, Roger D;Zhang, Shuguang;Lee, Richard T
• 通讯作者: Lee, Richard T

Local myocardial insulin-like growth factor 1 (IGF-1) delivery with biotinylated peptide nanofibers improves cell therapy for myocardial infarction.

• DOI: 10.1073/pnas.0602877103
• 发表时间: 2006-05-23
• 期刊: Proceedings of the National Academy of Sciences of the United States of America
• 影响因子: 11.1
• 作者: Michael E. Davis;P. Hsieh;Tomosaburo Takahashi;Q. Song;Shuguang Zhang;R. Kamm;A. Grodzinsky;P.
• 通讯作者: P.

Evidence from a genetic fate-mapping study that stem cells refresh adult mammalian cardiomyocytes after injury.

遗传命运图谱研究的证据表明，干细胞可以在成年哺乳动物心肌细胞受伤后恢复活力。

• 发表时间: 2007-08
• 影响因子: 82.9
• 作者: Hsieh, Patrick C H;Segers, Vincent F M;Davis, Michael E;MacGillivray, Catherine;Gannon, Joseph;Molkentin, Jeffery D;Robbins, Jeffrey;Lee, Richard T
• 通讯作者: Lee, Richard T

Endothelial cells promote cardiac myocyte survival and spatial reorganization: implications for cardiac regeneration.

内皮细胞促进心肌细胞存活和空间重组：对心脏再生的影响。

• 发表时间: 2004-08-24
• 影响因子: 37.8
• 作者: Narmoneva, Daria A;Vukmirovic, Rada;Davis, Michael E;Kamm, Roger D;Lee, Richard T
• 通讯作者: Lee, Richard T