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营养不良发育中大脑髓鞘形成不足机制中髓鞘特异性mRNA的下调

Down regulation of myelin-specific mRNAs in the mechanism of hypomyelination in the undernourished developing brain.

作者信息

Royland J, Konat G W, Kanoh M, Wiggins R C

机构信息

Department of Anatomy, School of Medicine, West Virginia University, Morgantown 26506.

出版信息

Brain Res Dev Brain Res. 1992 Feb 21;65(2):223-6. doi: 10.1016/0165-3806(92)90183-w.

DOI:10.1016/0165-3806(92)90183-w
PMID:1373995
Abstract

The expression of myelin-specific protein genes, i.e. myelin proteolipid (PLP), basic (BP), and myelin associated glycoproteins (MAG) was studied in normal and severely undernourished 20-day-old rats. The undernutrition paradigm resulted in reductions of approximately 50, 25 and 65% in body weight, brain weight and brain myelin yield, respectively. The amount of total brain RNA was not significantly altered, although the amount of cyclophilin (CYC) mRNA was increased. In contrast, the steady-state levels of myelin specific mRNAs were significantly decreased by approximately 40, 20 and 40% for PLP, BP and MAG, respectively. In addition, polyadenylation of the PLP transcript was altered, producing an abnormal ratio of the 1.6 kb to the 3.2 kb PLP mRNAs. The results indicate that down-regulation of myelin-specific gene expression is involved in the mechanisms of hypomyelination in hunger disease, although the individual genes are differently altered. Furthermore, undernutrition may have additional effects on the posttranscriptional processing of the transcripts as indicated by the abnormal size distribution of PLP messages.

摘要

在正常和严重营养不良的20日龄大鼠中,研究了髓鞘特异性蛋白基因,即髓鞘蛋白脂蛋白(PLP)、碱性蛋白(BP)和髓鞘相关糖蛋白(MAG)的表达。营养不良模型导致体重、脑重和脑髓鞘产量分别降低约50%、25%和65%。尽管亲环蛋白(CYC)mRNA的量增加,但总脑RNA的量没有显著改变。相比之下,PLP、BP和MAG的髓鞘特异性mRNA的稳态水平分别显著降低约40%、20%和40%。此外,PLP转录本的聚腺苷酸化发生改变,产生了1.6 kb与3.2 kb PLP mRNA的异常比例。结果表明,髓鞘特异性基因表达的下调参与了饥饿疾病中髓鞘形成不足的机制,尽管各个基因的改变有所不同。此外,如PLP信息的异常大小分布所示,营养不良可能对转录本的转录后加工有额外影响。

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