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

机译:通过上调粘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

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摘要

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.udud
机译:为了增强和调节对基于聚乳酸(PLLA)的材料的细胞亲和力,使用了两个亲水性配体聚乙二醇(PEG)和聚1-赖氨酸(PLL)来开发三嵌段共聚物:甲氧基封端的聚(乙二醇)-嵌段-聚(1-丙交酯)-嵌段-聚(1-赖氨酸)(MPEG-b-PLLA-b-PLL),以调节蛋白质的吸收和细胞粘附。在不同成分的MPEG-b-PLLA-b-PLL共聚物膜上培养骨髓基质细胞(BMSC),以确定修饰的聚合物表面对BMSC附着的影响。为了了解控制不同聚合物表面上初始细胞粘附的分子机制,使用定量逆转录酶聚合酶链反应(qRT-PCR)分析了84个人的细胞外基质(ECM)和粘附分子的mRNA表达。已发现粘附分子的下调是导致受损的BMSC在PLLA表面附着的原因。 MPEG-b-PLLA-b-PLL共聚物薄膜通过显着上调相关分子基因显着改善了细胞粘附和细胞骨架表达。六个粘附基因(CDH1,ITGL,NCAM1,SGCE,COL16A1和LAMA3)受修饰的PLLA表面影响最大。总之,聚合物表面改变了BMSCs的粘附分子基因表达,从而调节了修饰PLLA表面上的细胞初始附着。

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