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通过上调黏附分子基因增强人骨髓基质细胞对改性聚(L-丙交酯)表面的亲和力。

Enhanced human bone marrow stromal cell affinity for modified poly(L-lactide) surfaces by the upregulation of adhesion molecular genes.

机构信息

Institute of Health and Biomedical Innovation, Queensland University of Technology, 60 Musk Ave, Kelvin Grove Campus, Brisbane, QLD 4059, Australia.

出版信息

Biomaterials. 2009 Dec;30(36):6903-11. doi: 10.1016/j.biomaterials.2009.09.013. Epub 2009 Sep 30.

Abstract

To enhance and regulate cell affinity for poly (L-lactic acid) (PLLA) based materials, two hydrophilic ligands, poly (ethylene glycol) (PEG) and poly (L-lysine) (PLL), were used to develop triblock copolymers: methoxy-terminated poly (ethylene glycol)-block-poly (L-lactide)-block-poly (L-lysine) (MPEG-b-PLLA-b-PLL) in order to regulate protein absorption and cell adhesion. Bone marrow stromal cells (BMSCs) were cultured on different composition of MPEG-b-PLLA-b-PLL copolymer films to determine the effect of modified polymer surfaces on BMSC attachment. To understand the molecular mechanism governing the initial cell adhesion on difference polymer surfaces, the mRNA expression of 84 human extracellular matrix (ECM) and adhesion molecules was analysed using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). It was found that down regulation of adhesion molecules was responsible for the impaired BMSC attachment on PLLA surface. MPEG-b-PLLA-b-PLL copolymer films improved significantly the cell adhesion and cytoskeleton expression by upregulation of relevant molecule genes significantly. Six adhesion genes (CDH1, ITGL, NCAM1, SGCE, COL16A1, and LAMA3) were most significantly influenced by the modified PLLA surfaces. In summary, polymer surfaces altered adhesion molecule gene expression of BMSCs, which consequently regulated cell initial attachment on modified PLLA surfaces.

摘要

为了增强和调节聚(L-乳酸)(PLLA)基材料对细胞的亲和力,使用两种亲水配体,聚乙二醇(PEG)和聚(L-赖氨酸)(PLL),来开发嵌段共聚物:甲氧基封端的聚乙二醇-嵌段-聚(L-乳酸)-嵌段-聚(L-赖氨酸)(MPEG-b-PLLA-b-PLL),以调节蛋白质吸收和细胞黏附。将骨髓基质细胞(BMSCs)培养在不同组成的 MPEG-b-PLLA-b-PLL 共聚物膜上,以确定改性聚合物表面对 BMSC 黏附的影响。为了了解控制细胞在不同聚合物表面初始黏附的分子机制,使用定量逆转录聚合酶链反应(qRT-PCR)分析了 84 个人类细胞外基质(ECM)和黏附分子的 mRNA 表达。结果发现,黏附分子的下调是导致 PLLA 表面上 BMSC 黏附受损的原因。MPEG-b-PLLA-b-PLL 共聚物膜通过显著上调相关分子基因,显著改善了细胞黏附和细胞骨架表达。6 个黏附基因(CDH1、ITGL、NCAM1、SGCE、COL16A1 和 LAMA3)受改性 PLLA 表面的影响最大。总之,聚合物表面改变了 BMSCs 黏附分子基因的表达,从而调节了细胞在改性 PLLA 表面的初始黏附。

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