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: 8170960
• 负责人: Andrew J Putnam
• 金额: $ 4.15万
• 依托单位: UNIVERSITY OF CALIFORNIA-IRVINE
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-08-01 至 2011-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8170960
• 关键词: Actins; Blood capillaries; Computer Retrieval of Information on Scientific Projects Database; Fibrin; Funding; Grant; Hydrogels; Implant; Institution; Mediating; Modeling; Morphogenesis; PECAM1 gene; Research; Research Personnel; Resources; Source; Tissue Stains; Tissues; United States National Institutes of Health; angiogenesis; capillary; inhibitor/antagonist

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. 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 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 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。