Stiffness of Photocrosslinked RGD-Alginate Gels Regulates Adipose Progenitor Cell Behavior
Stiffness of Photocrosslinked RGD-Alginate Gels Regulates Adipose Progenitor Cell Behavior
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DOI：
10.1002/bit.23079
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发表时间：
2011-07-01
影响因子：
3.8
通讯作者：
Fischbach, Claudia
中科院分区：
文献类型：
--
作者：
Chandler, Emily M.;Berglund, Caroline M.;Fischbach, Claudia
脂肪祖细胞（APC）被广泛研究用于肿瘤切除后的软组织重建；然而，当前方法的长期成功仍然有限。为了开发临床相关的疗法，更好地了解细胞-微环境相互作用在脂肪组织再生中的作用至关重要。特别是，细胞外基质（ECM）力学对 APC 再生能力的影响仍有待阐明。我们使用基于光交联 RGD-藻酸盐的人工 ECM 来研究 3T3-L1 前脂肪细胞的脂肪生成和促血管生成潜力，作为基质硬度的函数。这些水凝胶使我们能够将基质硬度与粘附肽密度或细胞外 Ca2+ 浓度的变化解耦，并提供生理相关的 3D 培养背景。我们的研究结果表明，基质刚性的增加可促进 APC 自我更新和血管生成能力，但会抑制脂肪分化。总的来说，这项研究增进了我们对 ECM 力学在脂肪组织形成和血管化中作用的理解，并将有助于设计用于脂肪组织工程应用的有效生物材料支架。生物技术。生物工程。 2011； 108：1683-1692。 (C) 2011 年 Wiley 期刊公司。
Adipose progenitor cells (APCs) are widely investigated for soft tissue reconstruction following tumor resection; however, the long-term success of current approaches is still limited. In order to develop clinically relevant therapies, a better understanding of the role of cell-microenvironment interactions in adipose tissue regeneration is essential. In particular, the effect of extracellular matrix (ECM) mechanics on the regenerative capability of APCs remains to be clarified. We have used artificial ECMs based on photocrosslinkable RGD-alginate to investigate the adipogenic and pro-angiogenic potential of 3T3-L1 preadipocytes as a function of matrix stiffness. These hydrogels allowed us to decouple matrix stiffness from changes in adhesion peptide density or extracellular Ca2+ concentration and provided a physiologically relevant 3D culture context. Our findings suggest that increased matrix rigidity promotes APC self-renewal and angiogenic capacity, whereas, it inhibits adipose differentiation. Collectively, this study advances our understanding of the role of ECM mechanics in adipose tissue formation and vascularization and will aid in the design of efficacious biomaterial scaffolds for adipose tissue engineering applications. Biotechnol. Bioeng. 2011; 108: 1683-1692. (C) 2011 Wiley Periodicals, Inc.