ACTIN-MEDIATED CONTRACTILITY EFFECTS ON CAPILLARY MORPHOGENESIS IN TISSUES

肌动蛋白介导的组织毛细血管形态发生的收缩效应

• 批准号: 8365751
• 负责人: Andrew J Putnam
• 金额: $ 4.61万
• 依托单位: UNIVERSITY OF CALIFORNIA-IRVINE
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-08-20 至 2012-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8365751
• 关键词: Actins; Blood capillaries; Fibrin; Fluorescence; Funding; Grant; Hydrogels; Implant; Laboratories; Mediating; Modeling; Morphogenesis; National Center for Research Resources; PECAM1 gene; Principal Investigator; Research; Research Infrastructure; Resources; Source; Tissue Stains; Tissues; United States National Institutes of Health; angiogenesis; capillary; cost; inhibitor/antagonist

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. A bead-angiogenesis model is implanted in fibrin hydrogels of varied stiffness in this study. They are furthermore treated with actin contractility inhibitors. Angiogenic vessel sprouts that develop on the beads are then analyzed in terms of actin contractility presence as well as morphological differences. The tissues are stained for actin as well as CD31 to determine the effects of contractility inhibition on capillary morphogenesis.

这个子项目是许多利用资源的研究子项目之一 由NIH/NCRR资助的中心拨款提供。次级项目的主要支助 而子项目的主要调查员可能是由其他来源提供的， 包括其他NIH来源。 列出的子项目总成本可能 表示子项目使用的中心基础设施的估计数量， NCRR赠款不直接向子项目或子项目工作人员提供资金。 在这项研究中，珠血管生成模型植入不同刚度的纤维蛋白水凝胶。 它们还用肌动蛋白收缩抑制剂治疗。然后分析在珠上发展的血管生成血管芽的肌动蛋白收缩性存在以及形态学差异。 对组织进行肌动蛋白和CD 31染色，以确定收缩抑制对毛细血管形态发生的影响。