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.

该副本是利用资源的众多研究子项目之一 由NIH/NCRR资助的中心赠款提供。对该子弹的主要支持 而且，副投影的主要研究员可能是其他来源提供的 包括其他NIH来源。 列出的总费用可能 代表subproject使用的中心基础架构的估计量， NCRR赠款不直接向子弹或副本人员提供的直接资金。 在这项研究中，将珠血管生成模型植入了刚度各异的纤维蛋白水凝胶中。 此外，它们还接受了肌动蛋白收缩力抑制剂的治疗。然后，根据肌动蛋白的收缩力以及形态学差异来分析在珠子上发展的血管生成血管芽。 对肌动蛋白和CD31进行染色，以确定收缩力抑制对毛细血管形态发生的影响。