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Isolating the Effect of Stiffness on Valvular Interstitial Cells and its Role in Phenotype Control

机译:刚度对瓣膜间质细胞的影响及其在表型控制中的作用

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Our copolymer system with unvaried surface chemistry and controlled modulus show stiffness alone can change VIC behavior and induce osteoblastic differentiation, indicated by expression of the osteoblastic marker osteocalcin. without increasing aSMA. VIC expression of collagen on the surface of DEGDMA/nOM is significantly higher (8-15 fold) compared to osteoblastic and normal TCPS controls. ECM components are known to influence VIC phenotype and therefore the choice of substrate to invoke the correct ECM protein production in experimental systems is crucial. Interestingly the elastin profile (Fig 2D) and aSMA (data not shown) of our stiffest substrate does not mimic the OB control at day three, suggesting stiffness may cause VIC OB differentiation through an alternative pathway to traditional OB media induction.
机译:我们的共聚物系统具有不变的表面化学性质和受控的模量,显示出单独的刚度可以改变VIC行为并诱导成骨细胞分化,这由成骨细胞标志物骨钙素的表达所指示。而不会增加aSMA。与成骨细胞和正常TCPS对照相比,DEGDMA / nOM表面胶原蛋白的VIC表达明显更高(8-15倍)。已知ECM成分会影响VIC表型,因此选择底物以在实验系统中调用正确的ECM蛋白生产至关重要。有趣的是,我们最坚硬的基质的弹性蛋白谱(图2D)和aSMA(数据未显示)在第三天没有模仿OB控制,这表明僵硬可能通过传统OB培养基诱导的另一种途径导致VIC OB分化。

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