Perfusion and characterization of an endothelial cell-seeded modular tissue engineered construct formed in a microfluidic remodeling chamber.
Perfusion and characterization of an endothelial cell-seeded modular tissue engineered construct formed in a microfluidic remodeling chamber.
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DOI：
10.1016/j.biomaterials.2010.07.041
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发表时间：
2010-11
期刊：
影响因子：
14
通讯作者：
Sefton, Michael V.
中科院分区：
文献类型：
--
作者：
Khan, Omar F.;Sefton, Michael V.
关键词：
通过将内皮细胞接种的亚毫米大小的胶原圆柱体（模块）随机组装到微流体灌注室中，形成含有曲折内皮细胞内衬灌注通道的组织工程构建物。由随机模块包装产生的互连空隙空间产生了内衬有内皮细胞的流动通道。研究了通过迂曲通道的灌注（0.5 mL min-1，Re* = 14.36和剪切应力= 0.64 dyn cm-2）对结构重塑和内皮静止的影响。随着时间的推移，模块在其接触点处融合，并且随着它们收缩，减少了内部空隙空间，这减少了通过构造的整体灌注。与静态对照相比，灌注1小时后引起活化（ICAM-1和VCAM-1表达）的短暂增加，24小时后降低。增殖（BrdU）显着减少，而KLF 2，这是上调动脉粥样硬化保护层流剪切应力，24小时后显着上调。VE-钙粘蛋白变得不连续，并在24小时后显著下调，这可能是由于重塑过程中内皮细胞粘附连接的解体所致。总的来说，这些结果表明，通过构建体的流动不会将内皮细胞推向发炎的“动脉粥样硬化样”扰动流动病理。
Tissue engineered constructs containing tortuous endothelial cell-lined perfusion channels were formed by randomly assembling endothelial cell-seeded submillimeter-sized collagen cylinders (modules) into a microfluidic perfusion chamber. The interconnected void space produced by random module packing created flow channels that were lined with endothelial cells. The effect of perfusion (0.5 mL min−1, Re* = 14.36 and shear stress = 0.64 dyn cm−2) through the tortuous channels on construct remodeling and endothelium quiescence was studied. Over time, modules fused at their points of contact and as they contracted, decreased the internal void space, which reduced the overall perfusion through the construct. As compared to static controls, perfusion caused a transient increase in activation (ICAM-1 and VCAM-1 expression) after 1 hour followed by a decrease after 24 hours. Proliferation (by BrdU) was reduced significantly, while KLF2, which is upregulated with atheroprotective laminar shear stress, was upregulated significantly after 24 hours. VE-cadherin became discontinuous and was significantly downregulated after 24 hours, which was likely caused by the dismantling of the endothelial cell adherens junctions during remodeling. Collectively, these outcomes suggest that flow through the construct did not drive the endothelial cells towards an inflamed, “atherosclerotic like” disturbed flow pathology.
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影响因子：
6.1
作者：
Bruzewicz, Derek A.;McGuigan, Alison P.;Whitesides, George M.
通讯作者：
Whitesides, George M.
DOI：
10.1080/10623320210714
发表时间：
2002-01-01
期刊：
ENDOTHELIUM-NEW YORK
影响因子：
--
作者：
Imberti, B;Seliktar, D;Remuzzi, A
通讯作者：
Remuzzi, A
影响因子：
4.8
作者：
Hsiai, TK;Cho, SK;Ho, CM
通讯作者：
Ho, CM
影响因子：
56.9
作者：
LANGILLE, BL;ODONNELL, F
通讯作者：
ODONNELL, F
DOI：
10.1073/pnas.96.17.9815
发表时间：
1999-08-17
影响因子：
11.1
作者：
Corada, M;Mariotti, M;Dejana, E
通讯作者：
Dejana, E