National Engineering Laboratory for Modern Silk, College of Textile and Clothing Engineering, Soochow University, No. 199 Ren-ai Road, Suzhou Industrial Park, Suzhou, Jiangsu Province 215123, China.
Department of Ultrasonography, First Affiliated Hospital, Soochow University, Suzhou, Jiangsu 215006, China.
Mater Sci Eng C Mater Biol Appl. 2020 Sep;114:110977. doi: 10.1016/j.msec.2020.110977. Epub 2020 Apr 30.
Cell infiltration and proliferation are prerequisites for tissue regeneration and repair. The aim of the present study was to evaluate the motility and function of vascular smooth muscle cells (SMCs) in a silk-based small-caliber artificial blood vessel (SFTS) following implantation to replace the common carotid artery in rabbits. Hematoxylin and eosin (HE) staining showed a number of SMCs clearly distributed in the scaffold at 1 month, which gradually increased up to 80-90% of autologous blood vessels at 3 months and was 100% at 12 months. Smooth muscle myosin heavy chain (SM-MHC) and α-smooth muscle actin (α-SMA) are specific markers of SMCs. Real-time PCR results showed that the gene expression level of α-SMA in SFTSs was significantly down-regulated within 6 months, except in the early stage of implantation. The relative expression level of α-SMA at 12 months was five times higher than that at 3 months, indicating that SMCs phenotype transformed from synthetic to contractile. The SM-MHC+ and α-SMA+ SMCs were disorderly distributed in the scaffolds at 1 month, but became ordered along the circumference 6 months after grafting as shown by immunohistochemistry. Results indicated that the bionic SFTSs were able to induce in situ angiogenesis in defects.
细胞浸润和增殖是组织再生和修复的前提条件。本研究旨在评估植入兔颈总动脉后丝素基小口径人工血管(SFTS)中血管平滑肌细胞(SMC)的迁移和功能。苏木精和伊红(HE)染色显示,在 1 个月时,大量 SMC 明显分布在支架中,3 个月时逐渐增加到 80-90%的自体血管,12 个月时达到 100%。平滑肌肌球蛋白重链(SM-MHC)和α-平滑肌肌动蛋白(α-SMA)是 SMC 的特异性标志物。实时 PCR 结果显示,SFTS 中α-SMA 的基因表达水平在 6 个月内显著下调,除了在植入的早期阶段。12 个月时α-SMA 的相对表达水平是 3 个月时的 5 倍,表明 SMC 表型从合成型向收缩型转变。1 个月时 SM-MHC+和α-SMA+SMC 在支架中呈无序分布,但在移植 6 个月后,免疫组织化学显示它们沿圆周排列有序。结果表明,仿生 SFTS 能够在缺陷部位诱导原位血管生成。