Siironen J, Vuorio E, Sandberg M, Röyttä M
Department of Pathology, University of Turku, Finland.
J Peripher Nerv Syst. 1996;1(3):209-21.
Extracellular matrix changes are thought to be essential to the regeneration of peripheral nerves. The production of this matrix is believed to be regulated by interactions between axons and their supporting cells. In this study matrix production and cell proliferation were studied during rat sciatic nerve regeneration after a crush injury, and compared to that after rat sciatic nerve transection. Expression of proalpha1(I) and proalpha1(III) collagen and laminin beta1 mRNAs was followed in isolated endoneuria by Northern and in situ hybridization both proximally and distally to the site of either a crush injury or transection of rat sciatic nerve up to 18 weeks. Changes in the Schwann cell and fibroblast populations were monitored by morphometric analysis of endoneurial cross-sections immunostained for S-100 protein. The process of axonal regeneration was followed by Bielschowsky's silver staining. A crush injury initially resulted in increased expression of all mRNAs studied in the endoneurial cells. However, with progressing axonal regeneration the amount of collagen mRNAs returned to control levels, whereas the amount of laminin beta1 mRNA in the distal site of the crush remained elevated throughout the study period. The expression of type I collagen mRNA was enhanced after nerve transection injury compared to that after the crush injury. The epineurial fibroblasts actively expressed both type I and III collagen mRNAs after the injury. The proliferation of Schwann cells and the expression of collagen mRNAs are not, at least directly, related to the axonal regeneration. However, the long-lasting and strong expression of laminin beta1 mRNA after a nerve crush injury may be related to good axonal regeneration. The expression of type I collagen in the epineurium may lead to clinically well-recognized epineurial scarring and thus impede axonal regeneration.
细胞外基质的变化被认为是周围神经再生所必需的。这种基质的产生被认为受轴突与其支持细胞之间相互作用的调节。在本研究中，研究了大鼠坐骨神经挤压伤后再生过程中的基质产生和细胞增殖，并与大鼠坐骨神经横断伤后的情况进行了比较。通过Northern杂交和原位杂交，在分离的神经内膜中跟踪大鼠坐骨神经挤压伤或横断伤部位近端和远端直至18周的proalpha1(I)和proalpha1(III)胶原以及层粘连蛋白β1 mRNA的表达。通过对免疫染色为S-100蛋白的神经内膜横断面进行形态计量分析，监测雪旺细胞和成纤维细胞群体的变化。通过 Bielschowsky 银染色跟踪轴突再生过程。挤压伤最初导致神经内膜细胞中所有研究的mRNA表达增加。然而，随着轴突再生的进展，胶原mRNA的量恢复到对照水平，而挤压伤远端部位的层粘连蛋白β1 mRNA的量在整个研究期间保持升高。与挤压伤相比，神经横断伤后I型胶原mRNA的表达增强。损伤后，神经外膜成纤维细胞活跃地表达I型和III型胶原mRNA。雪旺细胞的增殖和胶原mRNA的表达至少直接与轴突再生无关。然而，神经挤压伤后层粘连蛋白β1 mRNA的长期强烈表达可能与良好的轴突再生有关。神经外膜中I型胶原的表达可能导致临床上公认的神经外膜瘢痕形成，从而阻碍轴突再生。
