ACTIN-MEDIATED CONTRACTILITY EFFECTS ON CAPILLARY MORPHOGENESIS IN TISSUES

这个子项目是利用资源的许多研究子项目之一。 由NIH/NCRR资助的中心拨款提供。对子项目的主要支持 子项目的首席调查员可能是由其他来源提供的， 包括美国国立卫生研究院的其他来源。为子项目列出的总成本可能 表示该子项目使用的中心基础设施的估计数量， 不是由NCRR赠款提供给次级项目或次级项目工作人员的直接资金。 本研究将珠状血管生成模型植入不同硬度的纤维蛋白水凝胶中。他们还接受肌动蛋白收缩抑制药的治疗。然后，根据肌动蛋白的收缩能力、存在以及形态差异来分析在珠子上生长的血管新生血管芽。对这些组织进行肌动蛋白和CD31染色，以确定收缩抑制对毛细血管形态发生的影响。

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.