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通过表面引发原子转移自由基聚合(SI-ATRP)控制基于整合素的对可降解电纺纤维支架的粘附。

Controlling integrin-based adhesion to a degradable electrospun fibre scaffold via SI-ATRP.

作者信息

Rodda Andrew E, Ercole Francesca, Glattauer Veronica, Nisbet David R, Healy Kevin E, Dove Andrew P, Meagher Laurence, Forsythe John S

机构信息

Department of Materials Science and Engineering, and Monash Institute for Medical Engineering, Monash University, Wellington Rd, Clayton 3800, Victoria, Australia.

出版信息

J Mater Chem B. 2016 Dec 7;4(45):7314-7322. doi: 10.1039/c6tb02444k. Epub 2016 Nov 3.

DOI:10.1039/c6tb02444k
PMID:32263733
Abstract

While polycaprolactone (PCL) and similar polyesters are commonly used as degradable scaffold materials in tissue engineering and related applications, non-specific adsorption of environmental proteins typically precludes any control over the signalling pathways that are activated during cell adhesion to these materials. Here we describe the preparation of PCL-based fibres that facilitate cell adhesion through well-defined pathways while preventing adhesion via adsorbed proteins. Surface-initiated atom transfer radical polymerisation (SI-ATRP) was used to graft a protein-resistant polymer brush coating from the surface of fibres, which had been electrospun from a brominated PCL macroinitiator. This coating also provided alkyne functional groups for the attachment of specific signalling molecules via the copper-mediated azide-alkyne click reaction; in this case, a cyclic RGD peptide with high affinity for αβ integrins. Mesenchymal stem cells were shown to attach to the fibres via the peptide, but did not attach in its absence, nor when blocked with soluble peptide, demonstrating the effective control of cell adhesion pathways.

摘要

虽然聚己内酯(PCL)和类似的聚酯通常用作组织工程及相关应用中的可降解支架材料,但环境蛋白质的非特异性吸附通常会妨碍对细胞黏附于这些材料时所激活的信号通路进行任何控制。在此,我们描述了基于PCL的纤维的制备方法,这些纤维通过明确的途径促进细胞黏附,同时防止通过吸附蛋白质进行黏附。表面引发的原子转移自由基聚合(SI-ATRP)用于从由溴化PCL大分子引发剂静电纺丝得到的纤维表面接枝抗蛋白质聚合物刷涂层。该涂层还提供了炔基官能团,用于通过铜介导的叠氮化物-炔基点击反应连接特定的信号分子;在这种情况下,是对αβ整合素具有高亲和力的环状RGD肽。间充质干细胞显示通过该肽附着于纤维,但在没有该肽时不附着,在用可溶性肽阻断时也不附着,这证明了对细胞黏附途径的有效控制。

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