Iihara K, Sasahara M, Hashimoto N, Hazama F
Department of Cerebrovascular Surgery, National Cardiovascular Center, Osaka, Japan.
J Cereb Blood Flow Metab. 1996 Sep;16(5):941-9. doi: 10.1097/00004647-199609000-00018.
Our previous study on the ischemia-induced expression of platelet-derived growth factor (PDGF)-B chain in the rat brain prompted us to examine expression of PDGF beta-receptor in the ischemic brain. Focal ischemia was induced by permanent tandem occlusion of middle cerebral and common carotid arteries in spontaneously hypertensive rats. Northern analysis revealed that ischemia significantly increased expression of the receptor in the ischemic neocortex at 4 and 7 days (328 +/- 109%; 323 +/- 119%, respectively, over control: n = 4, p < 0.05 versus sham). Neurons in infarct transiently showed increased immunostaining for the receptor at 1 day, whereas neurons in periinfarct area showed sustained and increased immunoreactivity from 1 to 14 days post-ischemia. Reactive glial cells in the external capsule and in molecular layer of the neocortex adjacent to infarct possessed enhanced immunoreactivity from 1 to 21 days. Furthermore, marked immunoreactivity was observed on brain macrophages in infarct and on the abluminal side of capillaries surrounding infarct from 4 to 7 days. These results demonstrated that ischemic insult increases expression of the PDGF beta-receptor at both the mRNA and protein level in the brain, suggesting its important role in cellular cascade of the ischemic brain.
我们之前关于大鼠脑缺血诱导血小板源性生长因子（PDGF）-B链表达的研究促使我们检测缺血脑中PDGFβ受体的表达。通过对自发性高血压大鼠永久性串联闭塞大脑中动脉和颈总动脉来诱导局灶性缺血。Northern印迹分析显示，缺血在第4天和第7天时显著增加了缺血性新皮质中该受体的表达（分别比对照组增加328±109%和323±119%：n = 4，与假手术组相比，p < 0.05）。梗死灶中的神经元在第1天时短暂显示出该受体免疫染色增加，而梗死灶周围区域的神经元在缺血后1至14天显示出持续且增加的免疫反应性。梗死灶外囊和邻近梗死灶的新皮质分子层中的反应性胶质细胞在1至21天具有增强的免疫反应性。此外，在第4至7天，在梗死灶中的脑巨噬细胞和梗死灶周围毛细血管的管腔外侧观察到明显的免疫反应性。这些结果表明，缺血性损伤增加了脑中PDGFβ受体在mRNA和蛋白质水平的表达，提示其在缺血性脑的细胞级联反应中起重要作用。
