期刊
BRAIN RESEARCH
卷 866, 期 1-2, 页码 286-298出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/S0006-8993(00)02240-X
关键词
TGF-beta 1immunoreactivity; hippocampal CA1 pyramidal neurons; microglia, astrocyte; transient forebrain ischemia; DNA fragmentation
Exogenous TGF-beta 1 has been shown to protect neurons from damage induced in vitro and in vivo. In this study we attempted to examine the expression of endogenous TGF-beta 1 mRNA and protein in the hippocampus of non-ischemic and ischemic rats, and to localize TGF-beta 1 protein and DNA fragmentation by double-staining. Transient ischemia was induced for 10 min in Wistar rats by clamping both common carotid arteries and lowering blood pressure to 40 mmHg. Bioactive TGF-beta 1 was selectively determined in CA1 pyramidal neurons of non-ischemic rats. It was upregulated after 3 h and 6 h of reperfusion corresponding to the increase in TGF-beta 1 RNA level detected by RT-PCR. Lectin and GFAP staining showed no detectable activated microglial cells and astrocytes in the hippocampus 3 h and 6 h after ischemia. When neuronal damage proceeded through day 2 to day 4 after ischemia as demonstrated by TUNEL-staining, TGF-beta 1 immunoreactivity (ir) disappeared in damaged neurons but persisted in viable neurons although TGF-beta 1 mRNA levels continuously increased. Double-staining revealed that TUNEL-positive neurons did not express TGF-beta 1 while TUNEL-negative neurons in the CA1 subfield exhibited a distinct TGF-beta 1 ir. These data indicate that hippocampal CA1 neurons can express TGF-beta 1 under physiological conditions and upregulate its expression during the first hours after ischemia, that is independent of the activation of glial cells. The endogenous TGF-beta 1 expressed in neurons may play a role in the pathological process of DNA degradation and delayed neuronal death after transient forebrain ischemia. (C) 2000 Elsevier Science B.V. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据