Tang Jin Bo, Xu Yan, Ding Fei, Wang Xiao Tian
Department of Hand Surgery, Hand Surgery Research Center, Affiliated Hospital of Nantong Medical College, Nantong, Jiangsu, China People's Republic of China.
J Hand Surg Am. 2004 Jul;29(4):564-70. doi: 10.1016/j.jhsa.2003.12.019.
Collagen production and reorientation are core events in the healing of tendons and are essential for gaining tensile strength. Intrasynovial flexor tendons are composed chiefly of type I collagen; however, type III collagen is the earliest to be laid down in the wounds. We investigated the expression of genes for type I collagen, type III collagen and its promoter, and nuclear transcription factor kappa B (NF-kappaB) in an in vivo tendon injury model in chickens.
Flexor digitorum profundus tendons of the long toes of 12 white leghorn chickens were transected partially and repaired with the modified Kessler method. The repaired tendon segments were harvested at 2, 4, and 8 weeks after surgery with 4 chickens used each time. The uninjured tendons from 4 other chickens were used as the controls. We determined the expression of the collagen and NF-kappaB genes in the tendons with reverse transcription and polymerase chain reaction and semiquantitative analysis of gene bands in gel electrophoresis.
Expression of the type III collagen gene was enhanced significantly in the tendons at 2, 4, and 8 weeks after repair. Levels of expression of the type III collagen promoter gene were increased significantly in the healing tendons at 2 and 4 weeks. Increases in the expression of the type I collagen gene occurred later than those of the type III collagen and NF-kappaB genes and were significant in the tendons after 4 and 8 weeks. The NF-kappaB gene was activated in the tendons at all the healing periods.
Expression of type III collagen and its promoter genes is enhanced remarkably during in vivo flexor tendon healing. The NF-kappaB gene is activated during the healing process. Expression of the type I collagen gene increases remarkably at later periods of in vivo tendon healing and is proportional to that of the NF-kappaB gene.
胶原蛋白的产生和重新定向是肌腱愈合的核心事件，对于获得抗张强度至关重要。滑膜内屈肌腱主要由I型胶原蛋白组成；然而，III型胶原蛋白是伤口中最早沉积的。我们在鸡的体内肌腱损伤模型中研究了I型胶原蛋白、III型胶原蛋白及其启动子以及核转录因子κB（NF-κB）的基因表达。
将12只白来航鸡长趾的趾深屈肌腱部分切断，采用改良Kessler法进行修复。每次用4只鸡，在术后2周、4周和8周收获修复的肌腱段。将另外4只鸡的未受伤肌腱用作对照。我们通过逆转录、聚合酶链反应以及凝胶电泳中基因条带的半定量分析来测定肌腱中胶原蛋白和NF-κB基因的表达。
修复后2周、4周和8周时，肌腱中III型胶原蛋白基因的表达显著增强。III型胶原蛋白启动子基因的表达水平在愈合肌腱的2周和4周时显著升高。I型胶原蛋白基因表达的增加比III型胶原蛋白和NF-κB基因晚，且在4周和8周后在肌腱中显著增加。NF-κB基因在所有愈合期的肌腱中均被激活。
在体内屈肌腱愈合过程中，III型胶原蛋白及其启动子基因的表达显著增强。NF-κB基因在愈合过程中被激活。I型胶原蛋白基因的表达在体内肌腱愈合后期显著增加，且与NF-κB基因的表达成正比。
