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首页> 外文期刊>Journal of Cellular Physiology >Roles of macrophage migration inhibitory factor in cartilage tissue engineering
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Roles of macrophage migration inhibitory factor in cartilage tissue engineering

机译：巨噬细胞迁移抑制因子的角色软骨组织工程

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To obtain stable outcomes in regenerative medicine, understanding and controlling immunological responses in transplanted tissues are of great importance. In our previous study, auricular chondrocytes in tissue‐engineered cartilage transplanted in mice were shown to express immunological factors, including macrophage migration inhibitory factor (MIF). Since MIF exerts pleiotropic functions, in this study, we examined the roles of MIF in cartilage regenerative medicine. We made tissue‐engineered cartilage consisting of auricular chondrocytes of C57BL/6J mouse, atellocollagen gel and a PLLA scaffold, and transplanted the construct subcutaneously in a syngeneic manner. Localization of MIF was prominent in cartilage areas of tissue‐engineered cartilage at 2 weeks after transplantation, though it became less apparent by 8 weeks. Co‐culture with RAW264 significantly increased the expression of MIF in chondrocytes, suggesting that the transplanted chondrocytes in tissue‐engineered cartilage could enhance the expression of MIF by stimulation of surrounding macrophages. When MIF was added in the culture of chondrocytes, the expression of type II collagen was increased, indicating that MIF could promote the maturation of chondrocytes. Meanwhile, toluidine blue staining of constructs containing wild type ( Mif+/+ ) chondrocytes showed increased metachromasia compared to MIF‐knockout ( Mif?/? ) constructs at 2 weeks. However, this tendency was reversed by 8 weeks, suggesting that the initial increase in cartilage maturation in Mif+/+ constructs deteriorated by 8 weeks. Since the Mif+/+ constructs included more iNOS‐positive inflammatory macrophages at 2 weeks, MIF might induce an M1 macrophage‐polarized environment, which may eventually worsen the maturation of tissue‐engineered cartilage in the long term.
机译：在再生获得稳定的结果医学、理解和控制在移植免疫反应组织是非常重要的。耳软骨细胞在组织工程软骨移植小鼠中表达免疫因素,包括巨噬细胞移动抑制因子(MIF)。自MIF施加多效性的功能,在这研究中,我们调查了MIF在软骨的角色再生医学。软骨组成的耳软骨细胞C57BL / 6 j小鼠,atellocollagen凝胶和丙交脂脚手架和移植的构造皮下注射同系的方式。本地化的MIF在软骨突出地理区域的组织工程软骨在2周移植后,尽管它变得更少通过8周明显。MIF的表达明显增加软骨细胞,这表明移植软骨细胞在组织工程软骨可能加强刺激的MIF的表达周围的巨噬细胞。文化的软骨细胞的表达II型胶原蛋白增加,表明MIF能促进软骨细胞的成熟。同时,甲苯胺蓝染色的结构含野生型(Mif + / +)软骨细胞显示异染色而增加MIF基因敲除应承担(MIF吗? / ?)然而,这种趋势被逆转8周,增加表明最初的软骨成熟的Mif + / +结构恶化8周。伊诺正炎性巨噬细胞在2周,MIF可能诱发M1巨噬细胞极化应承担的环境,这可能最终恶化的成熟组织工程软骨从长远来看。

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