ACTIN-MEDIATED CONTRACTILITY EFFECTS ON CAPILLARY MORPHOGENESIS IN TISSUES

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 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. 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.