ENHANCED EXPRESSION OF THE EXTRACELLULAR-MATRIX MOLECULE J1 TENASCIN IN THE REGENERATING ADULT-MOUSE SCIATIC-NERVE
ENHANCED EXPRESSION OF THE EXTRACELLULAR-MATRIX MOLECULE J1 TENASCIN IN THE REGENERATING ADULT-MOUSE SCIATIC-NERVE
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DOI：
10.1007/bf01257247
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发表时间：
1990-08-01
期刊：
影响因子：
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通讯作者：
FAISSNER, A
中科院分区：
文献类型：
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作者：
MARTINI, R;SCHACHNER, M;FAISSNER, A
我们通过免疫细胞学和免疫化学方法研究了正常和再生条件下成年小鼠坐骨神经中J1/tenascin的表达。在正常神经中，J1/肌腱蛋白表达仅限于 Ranvier 结和神经束膜的细胞外基质。神经横断后 2 天，在远端和近端神经残端的含有成纤维细胞的帽中、远端神经残端沿其整个长度以及近端神经残端的远端中可检测到 J1/腱生蛋白。在神经残端中，免疫反应性主要与由胶原纤维和施万细胞基底层组成的细胞外基质相关。横断后大约 7 天，神经残端的帽通常生长在一起形成桥。该桥由 J1/生腱蛋白阴性的神经束膜样结构和主要由成纤维细胞、内皮细胞和巨噬细胞组成的内部部分组成。该内部部分的所有细胞类型均嵌入 J1/肌腱蛋白阳性的胶原纤维基质中，指示神经元件的预期生长方向。几天后，桥中的 J1/腱生蛋白被限制在含有小雪旺细胞的神经束周围的细胞外基质中。在长期去神经支配 19 天的神经中，尽管雪旺细胞已渗透到远端残肢的帽中，但很难检测到 J1/腱生蛋白。损伤后大约 19 天，近端神经残端中的 J1/腱蛋白表达恢复到控制水平。在远端神经残端中，J1/肌腱蛋白免疫反应性在神经横断后约 14 天达到峰值，仅在约 35 天时消失，因此与轴突主动再生到远端神经残端的时间相关。这种减少被慢性去神经支配所阻止，这表明目标结构的神经支配可能与 J1/腱蛋白的下调有关。这些综合观察结果表明，J1/腱生蛋白在再生神经的各个部分受到差异性调节，可能是由不同的细胞和分子信号触发的。
We have investigated the expression of J1/tenascin in the sciatic nerve of the adult mouse under normal and regenerating conditions by immunocytological and immunochemical methods. In the normal nerve, J1/tenascin expression was confined to the extracellular matrix at the node of Ranvier and in the perineurium. At 2 days after nerve transection, J1/tenascin was detectable in the fibroblast-containing caps of the distal and proximal nerve stumps, in the distal nerve stump along its entire length and in the distal end of the proximal nerve stump. In the nerve stumps immunoreactivity was predominantly associated with extracellular matrix consisting of collagen fibrils and Schwann cell basal laminae. Approximately 7 days after transection, the caps of the nerve stumps has usually grown together forming a bridge. This bridge consisted of a J1/tenascin-negative perineurium-like structure and an inner part of predominantly fibroblasts, endothelial cells and macrophages. All cell types in this inner part were embedded in a J1/tenascin-positive matrix of collagen fibrils indicating the prospective direction of growth of neural elements. A few days later, J1/tenascin in the bridge was confined to the extracellular matrix around small Schwann cell-containing nerve fascicles. In nerves chronically denervated for 19 days, J1/tenascin was poorly detectable in the cap of the distal stump, although Schwann cells had infiltrated this cap. Approximately 19 days after the lesion, J1/tenascin expression returned to control levels in the proximal nerve stump. In the distal nerve stump, J1/tenascin immunoreactivity reached a peak at approximately 14 days after nerve transection and vanished only at approximately 35 days, thus correlating with the time of active regrowth of axons into the distal nerve stump. This reduction was prevented by chronic denervation, suggesting that reinnervation of target structures may be related to the down-regulation of J1/tenascin. These combined observations suggest that J1/tenascin is differentially regulated in the individual parts of the regenerating nerve, possibly triggered by different cellular and molecular signals.