CORRELATION BETWEEN ANGIOGENESIS AND BASIC FIBROBLAST GROWTH-FACTOR EXPRESSION IN EXPERIMENTAL BRAIN INFARCT
CORRELATION BETWEEN ANGIOGENESIS AND BASIC FIBROBLAST GROWTH-FACTOR EXPRESSION IN EXPERIMENTAL BRAIN INFARCT
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DOI：
10.1161/01.str.25.8.1651
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发表时间：
1994-08-01
期刊：
影响因子：
8.3
通讯作者：
LIU, HM
中科院分区：
文献类型：
--
作者：
CHEN, HH;CHIEN, CH;LIU, HM
背景与目的正常情况下，脑内皮细胞处于静止状态；它们被刺激在梗死周围增殖，尽管其机制尚不清楚。在本研究中，我们通过脑梗死参与细胞探讨了血管生成与碱性成纤维细胞生长因子（bFGF）表达的关系。方法结扎大鼠左大脑中动脉分支，永久性阻断左颈总动脉，暂时性阻断右颈总动脉，造成脑梗死。1 ~ 14 d后取脑组织，用组织学和免疫组织化学方法进行研究。溴脱氧尿苷（BRdU）作为增殖细胞的s期标记物。结果1天后，梗死灶附近神经元的bFGF免疫反应性增强，并随之向远端同侧半球神经元扩散。2天后，梗死周围的血管和神经胶质细胞开始掺入BRdU。在第一周内，新的毛细血管伴随着巨噬细胞延伸到梗死区。巨噬细胞、内皮细胞和反应性星形胶质细胞表达轻度至中度bFGF免疫反应性。结论bFGF表达与血管生成的时空相关性以及bFGF众所周知的生物学特性提示，神经元、巨噬细胞和胶质细胞产生的bFGF可能参与脑梗死血管生成。
Background and Purpose Cerebral endothelial cells are quiescent under normal conditions; they are stimulated to proliferate around an infarct, although the mechanism is unclear. In the present study we explored the relation between angiogenesis and the expression of basic fibroblast growth factor (bFGF) by participating cells in brain infarct.Methods Brain infarct was created in rats by ligation of a branch of the left middle cerebral artery followed by permanent occlusion of the left common carotid artery and temporary occlusion of the right common carotid artery. The brains were removed after 1 to 14 days and studied with histological and immunohistochemical methods. Bromodeoxyuridine (BRdU) was used as an S-phase marker for the proliferative cells.Results Enhanced bFGF immunoreactivity was observed in neurons adjacent to the infarct after 1 day, and the change subsequently spread to distant neurons in the ipsilateral hemisphere. After 2 days blood vessels and glial cells around the infarct began to incorporate BRdU. During the first week new capillaries accompanied by macrophages extended into the infarct. The macrophages, endothelial cells, and reactive astrocytes expressed mild to moderate bFGF immunoreactivity.Conclusions The spatial and temporal correlation between bFGF expression and angiogenesis in conjunction with the well-known biological properties of bFGF suggest that bFGF produced by neurons, macrophages, and glial cells may participate in angiogenesis in brain infarct.