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Ina M. Wittko-Schneider Fabian T. Schneider Karl H. Plate 《Cellular and molecular life sciences : CMLS》2013,70(10):1705-1725
Vascular endothelial growth factors (VEGFs), initially thought to act specifically on the vascular system, exert trophic effects on neural cells during development and adulthood. Therefore, the VEGF system serves as a promising therapeutic target for brain pathologies, but its simultaneous action on vascular cells paves the way for harmful side effects. To circumvent these deleterious effects, many studies have aimed to clarify whether VEGFs directly affect neural cells or if the effects are mediated secondarily via other cell types, like vascular cells. A great number of reports have shown the expression and function of VEGF receptors (VEGFRs), mainly VEGFR-1 and -2, in neural cells, where VEGFR-2 has been described as the major mediator of VEGF-A signals. This review aims to summarize and compare the divergent roles of VEGFR-1 and -2 during CNS development and homeostasis. 相似文献
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Vascular endothelial growth factor is a potential tumour angiogenesis factor in human gliomas in vivo. 总被引:106,自引:0,他引:106
Clinical and experimental studies suggest that angiogenesis is a prerequisite for solid tumour growth. Several growth factors with mitogenic or chemotactic activity for endothelial cells in vitro have been described, but it is not known whether these mediate tumour vascularization in vivo. Glioblastoma, the most common and most malignant brain tumour in humans, is distinguished from astrocytoma by the presence of necroses and vascular proliferations. Here we show that expression of an endothelial cell-specific mitogen, vascular endothelial growth factor (VEGF), is induced in astrocytoma cells but is dramatically upregulated in two apparently different subsets of glioblastoma cells. The high-affinity tyrosine kinase receptor for VEGF, flt, although not expressed in normal brain endothelium, is upregulated in tumour endothelial cells in vivo. These observations strongly support the concept that tumour angiogenesis is regulated by paracrine mechanisms and identify VEGF as a potential tumour angiogenesis factor in vivo. 相似文献
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本文介绍了逐差法处理物理实验数据的基本方法和适用范围,表明了逐差法处理实验数据的优点. 相似文献
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Deletion of the hypoxia-response element in the vascular endothelial growth factor promoter causes motor neuron degeneration 总被引:35,自引:0,他引:35
Oosthuyse B Moons L Storkebaum E Beck H Nuyens D Brusselmans K Van Dorpe J Hellings P Gorselink M Heymans S Theilmeier G Dewerchin M Laudenbach V Vermylen P Raat H Acker T Vleminckx V Van Den Bosch L Cashman N Fujisawa H Drost MR Sciot R Bruyninckx F Hicklin DJ Ince C Gressens P Lupu F Plate KH Robberecht W Herbert JM Collen D Carmeliet P 《Nature genetics》2001,28(2):131-138
Hypoxia stimulates angiogenesis through the binding of hypoxia-inducible factors to the hypoxia-response element in the vascular endothelial growth factor (Vegf) promotor. Here, we report that deletion of the hypoxia-response element in the Vegf promotor reduced hypoxic Vegf expression in the spinal cord and caused adult-onset progressive motor neuron degeneration, reminiscent of amyotrophic lateral sclerosis. The neurodegeneration seemed to be due to reduced neural vascular perfusion. In addition, Vegf165 promoted survival of motor neurons during hypoxia through binding to Vegf receptor 2 and neuropilin 1. Acute ischemia is known to cause nonselective neuronal death. Our results indicate that chronic vascular insufficiency and, possibly, insufficient Vegf-dependent neuroprotection lead to the select degeneration of motor neurons. 相似文献
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