Forebrain ischemia increases GLUT1 protein in brain microvessels and parenchyma.
Forebrain ischemia increases GLUT1 protein in brain microvessels and parenchyma.
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前脑缺血会增加脑微血管和实质中的 GLUT1 蛋白。
DOI：
10.1097/00004647-199601000-00008
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Lessov,N
中科院分区：
文献类型：
--
作者：
McCall,AL;VanBueren,AM;Nipper,V;Moholt-Siebert,M;Downes,H;Lessov,N
将葡萄糖转运到非神经元脑细胞中使用葡萄糖转运蛋白GLUT 1的不同糖基化形式。微血管GLUT 1在免疫细胞化学上很容易观察到，尽管它的实质定位很困难。缺血后，GLUT 1 mRNA增加，但GLUT 1蛋白是否也发生变化尚不确定。因此，我们研究了GLUT 1在正常大鼠脑和短暂性全前脑缺血后的免疫细胞化学分布。一个新的免疫细胞化学发现是肽可识别的GLUT 1免疫反应性染色的实质，以及在脑微血管。在非缺血性大鼠，脑实质GLUT 1染色共定位与胶质细胞酸性蛋白（GFAP）在血管周围足的星形胶质细胞的过程。缺血后24小时，微血管和非微血管GLUT 1免疫反应性广泛增加，持续在4天后缺血。脑缺血后，脑切片内的血管密度也同样增加。胶质纤维酸性蛋白染色证实脑实质GLUT 1表达增加，提示非血管性GLUT 1过表达可能发生在反应性星形胶质细胞。最后观察到诱导热休克蛋白（HSP）70在海马和皮质缺血后24小时的快速表达。我们的结论是，GLUT 1通常是免疫细胞化学检测脑微血管和实质和实质表达发生在一些星形胶质细胞。全脑缺血后，GLUT 1过表达在微血管和脑实质中迅速而广泛地发生;其过表达可能与细胞应激反应的立即早期基因形式有关。
Glucose transport into nonneuronal brain cells uses differently glycosylated forms of the glucose transport protein, GLUT1. Microvascular GLUT1 is readily seen on immunocytochemistry, although its parenchymal localization has been difficult. Following ischemia, GLUT1 mRNA increases, but whether GLUT1 protein also changes is uncertain. Therefore, we examined the immunocytochemical distribution of GLUT1 in normal rat brain and after transient global forebrain ischemia. A novel immunocytochemical finding was peptide-inhibitable GLUT1 immunoreactive staining in parenchyma as well as in cerebral microvessels. In nonischemic rats, parenchymal GLUT1 staining co-localizes with glial fibrillary acidic protein (GFAP) in perivascular foot processes of astrocytes. By 24 h after ischemia, both microvascular and nonmicrovascular GLUT1 immunoreactivity increased widely, persisting at 4 days postischemia. Vascularity within sections of brain similarly increased after ischemia. Increased parenchymal GLUT1 expression was paralleled by staining for GFAP, suggesting that nonvascular GLUT1 overexpression may occur in reactive astrocytes. A final observation was a rapid expression of inducible heat shock protein (HSP)70 in hippocampus and cortex by 24 h after ischemia. We conclude that GLUT1 is normally immunocytochemically detectable in cerebral microvessels and parenchyma and that parenchymal expression occurs in some astroglia. After global cerebral ischemia, GLUT1 overexpression occurs rapidly and widely in microvessels and parenchyma; its overexpression may be related to an immediate early-gene form of response to cellular stress.