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首页> 外文期刊>Biomaterials >Myofibroblastic activation of valvular interstitial cells is modulated by spatial variations in matrix elasticity and its organization
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Myofibroblastic activation of valvular interstitial cells is modulated by spatial variations in matrix elasticity and its organization

机译：通过基质弹性的空间变化及其组织的空间变化来调节瓣膜间质细胞的肌纤维模粒激活

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VICs Valvular interstitial cells (VICs) are key regulators of the heart valve's extracellular matrix (ECM), and upon tissue damage, quiescent VIC fibroblasts become activated to myofibroblasts. As the behavior of VICs during disease progression and wound healing is different compared to healthy tissue, we hypothesized that the organization of the matrix mechanics, which results from depositing of collagen fibers, would affect VIC phenotypic transition. Specifically, we investigated how the subcellular organization of ECM mechanical properties affects subcellular localization of Yes-associated protein (YAP), an early marker of mechanotransduction, and alpha-smooth muscle actin (alpha-SMA), a myofibroblast marker, in VICs. Photo-tunable hydrogels were used to generate substrates with different moduli and to create organized and disorganized patterns of varying elastic moduli. When porcine VICs were cultured on these matrices, YAP and alpha-SMA activation were significantly increased on substrates with higher elastic modulus or a higher percentage of stiff regions. Moreover, VICs cultured on substrates with a spatially disorganized elasticity had smaller focal adhesions, less nuclear localized YAP, less alpha-SMA organization into stress fibers and higher proliferation compared to those cultured on substrates with a regular mechanical organization. Collectively, these results suggest that disorganized spatial variations in mechanics that appear during wound healing and fibrotic disease progression may influence the maintenance of the VIC fibroblast phenotype, causing more proliferation, ECM remodeling and matrix deposition. (C) 2017 Elsevier Ltd. All rights reserved.
机译：VICS瓣膜间质细胞（VICS）是心脏瓣膜细胞外基质（ECM）的关键稳压器，并且在组织损伤时，静止的VIC成纤维细胞被激活到肌纤维细胞上。随着疾病进展和伤口愈合期间的vics的行为与健康组织相比不同，我们假设基质力学的组织，这导致胶原纤维沉积，会影响VIC表型转变。具体地，我们研究了ECM机械性能的亚细胞组织如何影响Yes相关蛋白（YAP）的亚细胞定位，机械调节的早期标记，以及α-平滑肌肌动蛋白（α-SMA），肌纤维细胞标志物中的雌蕊肌肌肌肌肌肌肌肌肌肌肌肌肌肌蛋白质中的亚型蛋白质中。光可调水凝胶用于产生具有不同模量的基材，并产生各种弹性模量的有组织和杂化模式。当在这些基质上培养猪的培养物时，在具有较高弹性模量的基板上或较高的刚性区域的底物上显着增加了YAP和α-SMA活化。此外，与空间紊乱弹性的底物上培养的VIC具有较小的焦粘连，核局部化yap，较少的α-SMA组织，与具有常规机械组织的衬底上培养的那些相比，较高的α-SMA组织和更高的增殖。这些结果表明，伤口愈合期间出现的力学的紊乱空间变化可能影响维护纤维细胞表型的维持，导致更多的增殖，ECM重塑和基质沉积。 （c）2017 Elsevier Ltd.保留所有权利。

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