Li X, Gu W, Masinde G, Hamilton-Ulland M, Xu S, Mohan S, Baylink D J
Molecular Genetics Division, Musculoskeletal Disease Center, JL Pettis VA Medical Center and Loma Linda University, Loma Linda, CA 92357, USA.
Heredity (Edinb). 2001 Jun;86(Pt 6):668-74. doi: 10.1046/j.1365-2540.2001.00879.x.
There have been few studies of the inheritance of wound healing in mammals. In this study, we demonstrate that inbred strains of mice differ significantly in the rate of wound healing. Of the 20 strains tested, fast healers (MRL/MpJ-Fas(lpr) and LG/J) healed wounds four times faster than slow healers (Balb/cByJ and SJL/J). The genetic basis underlying the difference in the healing capacity was analysed using F2 populations of two different crosses. We show that the wound healing is a polygenically determined quantitative trait with an average estimated heritability of 86%. The modes of gene action in these two crosses are different. In the (MRL/MpJ x SJL/J) cross, genes regulating fast healing in MRL/MpJ mice exhibited additive effects, whereas these effects were suppressed by a dominant repressor gene in CBA/J mice in the (MRL/MpJ-Fas(lpr) x CBA/J) cross. Information gained from this investigation provides insight into further study of molecular mechanisms underlying the rate of wound healing in mammals.
关于哺乳动物伤口愈合遗传情况的研究很少。在本研究中，我们证明近交系小鼠在伤口愈合速度上存在显著差异。在测试的20个品系中，愈合快的品系（MRL/MpJ-Fas(lpr)和LG/J）伤口愈合速度比愈合慢的品系（Balb/cByJ和SJL/J）快四倍。利用两个不同杂交组合的F2群体分析了愈合能力差异的遗传基础。我们表明伤口愈合是一个由多基因决定的数量性状，平均估计遗传力为86%。这两个杂交组合中的基因作用模式不同。在（MRL/MpJ×SJL/J）杂交中，调控MRL/MpJ小鼠快速愈合的基因表现出加性效应，而在（MRL/MpJ-Fas(lpr)×CBA/J）杂交中，这些效应被CBA/J小鼠中的一个显性抑制基因所抑制。从这项研究中获得的信息为进一步研究哺乳动物伤口愈合速度的分子机制提供了见解。
