Induction of thymosin beta(4) mRNA following focal brain ischemia

被引:51
|
作者
Vartiainen, N
Pyykonen, I
Hokfelt, T
Koistinaho, J
机构
[1] UNIV KUOPIO,AI VIRTANEN INST,FIN-70211 KUOPIO,FINLAND
[2] UNIV TAMPERE,SCH MED,FIN-33101 TAMPERE,FINLAND
[3] KAROLINSKA INST,DEPT NEUROSCI,S-17177 STOCKHOLM,SWEDEN
关键词
neuronal plasticity; gene regulation; brain ischaemia; actin polymerization; mRNA;
D O I
10.1097/00001756-199607080-00017
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
THYMOSIN beta 4 is a protein expressed in most rodent and human tissues, including the brain, and is thought to participate in neurite outgrowth during development by sequestration of G-actin necessary for growth cone extension Under normal conditions in the adult rat brain, the gene has been suggested to be expressed in microglia and CA1-CA2 hippocampal pyramidal cells. Here we show by using in situ hybridization that t beta 4 is dramatically up-regulated in the infarcted brain area after focal ischaemia. In addition, moderate t beta 4 induction is detected in the perifocal zone, substantia nigra and CA1-CA3 hippocampal pyramidal neurones. Macrophages are probably responsible for t beta 4 induction in the infarcted region, and activated non-neuronal cells probably contribute to the induction seen in the thalamus, substantia nigra and perifocal zone. However, the pyramidal neurones in the hippocampus show t beta(4) upregulation which may be related to restoration of neurite circuits after focal ischemic damage.
引用
收藏
页码:1613 / 1616
页数:4
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