Regulation of Macrophage Migration Inhibitory Factor ForHealing of Tendons and Ligaments

巨噬细胞移动抑制因子（MIF）在韧带损伤后修复过程中的表达及其作用的研究尚未见报道。本研究旨在验证MIF基因缺陷可能延迟内侧副韧带（MCL）愈合的假说。本研究表明，在损伤后第28天，MIF基因缺陷小鼠（MIFKO）的愈合组织中的机械性能和基质金属蛋白酶（MMP）-2和13 mRNA的水平显著低于野生型小鼠（WT）。在组织学上，与WT相比，MIFKO中的愈合组织表现出延长的肥大、不良的血管分布和延长的细胞数量增加。综上所述，提示MIFKO表现出MCL的延迟愈合，这可能是由MMP-2和-13的较低mRNA表达引起的。

There have been no reports that investigated the expression or the role of macrophage migration inhibitory factor (MIF) in the repair process after ligament injury. The aim of this study was to test the hypothesis that that the deficiency in MIF gene might delay medial collateral ligament (MCL) healing. The present study showed that the levels of mechanical properties and matrix metalloproteinase (MMP)-2 and -13 mRNA in the healing tissue were significantly lower in MIF gene-deficient mice (MIFKO) than in wild-type mice (WT) on day 28 after injury. Histologically, healing tissues in MIFKO exhibited prolonged hypertrophy, poor vascularity, and prolonged increase in cell number compared with those in WT. Taken together, it was suggested that MIFKO exhibited delayed healing of the MCL, which might be caused by lower mRNA expression of MMP-2 and -13.