Yrigoin Ksenia, Bernard Kaitlyn N, Castaño Maria A, Cleaver Ondine, Sumanas Saulius, Davis George E
Department of Molecular Pharmacology and Physiology, Morsani College of Medicine, University of South Florida, Tampa, FL, United States.
Department of Molecular Biology, UT Southwestern School of Medicine, Dallas, TX, United States.
Front Cell Dev Biol. 2024 Oct 31;12:1465806. doi: 10.3389/fcell.2024.1465806. eCollection 2024.
In this study, we identify and characterize new molecular determinants that optimize human capillary tube network assembly. Our lab has previously reported a novel, serum free-defined 3D co-culture model using human endothelial cells (ECs) and human pericytes whereby EC-lined tubes form and co-assemble with pericytes, but when these cultures are maintained at or beyond 5 days, tubes become progressively wider and unstable. To address this issue, we generated novel human pericytes that carry a tissue inhibitor of metalloproteinase (TIMP)-3 transgene which can be upregulated following doxycycline addition. EC-pericyte co-cultures established in the presence of doxycycline demonstrated marked enhancement of capillary network assembly including dramatic narrowing of capillary tube widths to an average of 8 µm (physiologic capillary tube width), increased tube lengths, increased tube branching, and robust stimulation of basement membrane matrix assembly, particularly with collagen type IV and fibronectin deposition compared to controls. These substantial changes depend not only on induction of pericyte TIMP-3, but also on recruitment of pericytes to EC tubes. Blockade of pericyte recruitment prevents these dramatic capillary network alterations suggesting that EC-pericyte interactions and induction of pericyte TIMP-3 are necessary together to coordinate and facilitate capillary assembly and maturation. Overall, this work is critical for our basic understanding of capillary formation, but also for the ability to reproducibly generate stabilized networks of capillary tubes.
在本研究中,我们鉴定并表征了优化人类毛细血管网络组装的新分子决定因素。我们实验室此前报道了一种新型的、无血清定义的三维共培养模型,该模型使用人类内皮细胞(ECs)和人类周细胞,在此模型中,内皮细胞衬里的管形成并与周细胞共同组装,但当这些培养物维持5天及以上时,管会逐渐变宽且不稳定。为了解决这个问题,我们生成了携带金属蛋白酶组织抑制剂(TIMP)-3转基因的新型人类周细胞,该转基因在添加强力霉素后可上调。在强力霉素存在下建立的内皮细胞-周细胞共培养显示出毛细血管网络组装的显著增强,包括毛细血管管宽度显著变窄至平均8微米(生理毛细血管管宽度)、管长度增加、管分支增加,以及基底膜基质组装的强烈刺激,特别是与对照组相比,IV型胶原蛋白和纤连蛋白沉积增加。这些显著变化不仅取决于周细胞TIMP-3的诱导,还取决于周细胞向内皮细胞管的募集。阻断周细胞募集可防止这些显著的毛细血管网络改变,这表明内皮细胞-周细胞相互作用和周细胞TIMP-3的诱导共同是协调和促进毛细血管组装和成熟所必需的。总体而言,这项工作对于我们对毛细血管形成的基本理解至关重要,对于可重复生成稳定的毛细血管管网的能力也至关重要。