Vascular endothelial growth factor upregulation in transient global ischemia induced by cardiac arrest and resuscitation in rat brain

Vascular endothelial growth factor upregulation in transient global ischemia induced by cardiac arrest and resuscitation in rat brain
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DOI:
10.1016/s0169-328x(99)00261-2
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发表时间:
1999-12-10
期刊:
MOLECULAR BRAIN RESEARCH
影响因子:
--
通讯作者:
LaManna, JC
LaManna, JC
中科院分区:
其他
文献类型:
--
作者:
Pichiule, P;Chávez, JC;LaManna, JC

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本研究检测了心脏骤停和复苏产生的可逆性全脑缺血大鼠脑血管内皮生长因子(VEGF)的表达。RT-PCR分析显示VEGF在皮质、海马和脑干中有188、164和120个可变剪接形式。在从心脏骤停恢复24小时后,在分析的所有区域中,对应于VEGF(188)和VEGF(164)的mRNA水平显著增加约一倍。这些mRNA水平在恢复后24和48 h仍保持升高,但在恢复后7天恢复至基础表达。心脏骤停后VEGF(120)表达的变化没有达到统计学意义。通过Western印迹法测量的VEGF蛋白表达在恢复24和48小时也增加了约一倍,但在恢复7天后恢复至对照水平。VEGF免疫组化定位这种表达增加主要与星形胶质细胞相关。考虑到其生物学活性,心脏骤停和复苏后的VEGF诱导可能是可逆性全脑缺血后24-48 h发现的血管通透性增加和由此产生的血管源性水肿的原因。(C)1999 Elsevier Science B. V.保留所有权利。
This study examined vascular endothelial growth factor (VEGF) expression in rat brain after reversible global cerebral ischemia produced by cardiac arrest and resuscitation. Three alternative splicing forms, VEGF(188), VEGF(164) and VEGF(120), were observed in cortex, hippocampus and brainstem by RT-PCR analysis. After 24 h of recovery from cardiac arrest, mRNA levels corresponding to VEGF(188) and VEGF(164) were significantly increased by about double in all the regions analyzed. These mRNA levels remained elevated at 24 and 48 h of recovery but returned to basal expression after 7 days of recovery. Changes in VEGF(120) expression after cardiac arrest did not reach statistical significance. VEGF protein expression measured by Western blot was also increased by about double at 24 and 48 h of recovery but returned to control levels after 7 days of recovery. VEGF immunohistochemistry localized this increased expression mostly associated with astrocytes. Considering its biological activity, VEGF induction after cardiac arrest and resuscitation may be responsible for the increased vascular permeability and the resultant vasogenic edema, found 24-48 h after reversible global ischemia. (C) 1999 Elsevier Science B.V. All rights reserved.