Myelin-associated glycoprotein gene expression in the presence and absence of Schwann cell-axonal contact.
Myelin-associated glycoprotein gene expression in the presence and absence of Schwann cell-axonal contact.
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存在和不存在雪旺细胞轴突接触时髓磷脂相关糖蛋白基因的表达。
DOI：
10.1159/000111832
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发表时间：
1990
影响因子：
2.9
通讯作者：
Mezei,C
中科院分区：
文献类型：
--
作者：
Gupta,SK;Poduslo,JF;Dunn,R;Roder,J;Mezei,C
挤压损伤和永久切断的坐骨神经远端段分别提供了研究雪旺细胞-轴突接触和不接触雪旺细胞活动的模型。我们在挤压伤后3周和横断后35天检测了髓鞘相关糖蛋白(MAG)编码转录本的数量和质量，以探讨该基因在神经损伤和后续修复中的可能调节。Northern印迹和狭缝印迹分析表明，挤压伤后2天MAG mRNA表达水平急剧下降，7~21天后，MESSAGE表达水平逐渐升高。Western印迹分析显示，挤压伤后7天MAG蛋白水平显著下降，伤后21天恢复到成人值的70%。在坐骨神经永久切断后35d，Northern和Western分析均未检测到MAG基因和蛋白的表达。这意味着周围神经永久切断后MAG基因的表达明显下调。这些对MAG转录本和编码蛋白的比较研究表明，在这些周围神经疾病的实验模型中，MAG基因的表达在转录水平上受到调控，也可能在转录后水平上受到调控。
The distal segments of the crush-injured and permanently transected sciatic nerve provide models to study Schwann cell activity in the presence and absence of Schwann cell-axonal contact, respectively. We examined the quantity and quality of transcript coding for the myelin-associated glycoprotein (MAG) over a 3-week period following crush injury and at 35 days after transection to investigate possible regulation of this gene during nerve injury and subsequent repair. Northern blot and slot blot analysis indicated a sharp decrease in levels of MAG mRNA 2 days after crush injury which was followed by a progressive increase in levels of message between 7 and 21 days after injury. Western blot analysis showed that levels of MAG protein decreased substantially 7 days after crush injury, which returned to 70% of the adult value by 21 days after injury. MAG mRNA and protein were undetectable by Northern and Western analysis, respectively, in the distal segment of the sciatic nerve 35 days after permanent transection. This infers distinct down-regulation of MAG gene expression after permanent transection of a peripheral nerve. These comparative studies of MAG transcripts and encoded protein may indicate regulation of MAG gene expression at the level of transcription, and possibly at the level of post-transcription in these experimental models of peripheral neuropathies.