Abstract
Vascular endothelial growth factor (VEGF) is well known as the growth factor with wide-ranging functions even in the central nervous system (CNS). Presently, most attention is given to the investigation of its role in neuronal protection, growth and maturation processes, whereby most effects are mediated through VEGF receptor 2 (VEGFR-2). The purpose of our current study is to provide new insights into the impact of VEGF on immature and mature Purkinje cells (PCs) in accordance with maturity and related receptor expression. Therefore, to expand our knowledge of VEGF effects in PCs development and associated VEGFR-2 expression, we used cultivated organotypic cerebellar slice cultures in immunohistochemical or microinjection studies, followed by confocal laser scanning microscopy (CLSM) and morphometric analysis. Additionally, we incorporated in our study the method of laser microdissection, followed by quantitative polymerase chain reaction (qPCR). For the first time we could show the age-dependent VEGF sensitivity of PCs with the largest promoting effects being on dendritic length and cell soma size in neonatal and juvenile stages. Once mature, PCs were no longer susceptible to VEGF stimulation. Analysis of VEGFR-2 expression revealed its presence in PCs throughout development, which underlined its mediating functions in neuronal cells.
Highlights
Senger et al (1983) first described the vascular endothelial growth factor (VEGF) as a tumorsecreted vascular permeability protein
One aim of the current study was to investigate, whether dendritogenesis, somatogenesis and spinogenesis in neonatal, juvenile and mature Purkinje cells (PCs) can be stimulated by Vascular endothelial growth factor (VEGF). Besides this we investigated the differential expression of VEGF receptor 2 (VEGFR-2) in neonatal, juvenile and adult PCs by employing methods of immunohistochemistry, in situ hybridization and laser microdissection, followed by quantitative polymerase chain reaction
At this point of time granule cells GCs migrate from the external granule cell layer (eGCL) through the molecular cell layer (MCL) and Purkinje cell layer (PCL) to generate the inner granule cell layer (GCL), with its migration peak at p10-11 (Altman, 1972; Kunimoto and Suzuki, 1997), and its end after 16 days of maturation (Mancini et al, 2009)
Summary
Senger et al (1983) first described the vascular endothelial growth factor (VEGF) as a tumorsecreted vascular permeability protein. VEGF molecules are able to bind to different receptors such as VEGFR-1, -2 (KDR,) and -3 (FLT-1, FLK-1, FLT-4), which belong to the family of receptor tyrosin kinases (Neufeld et al, 1999). These transmembrane proteins contain a tyrosin kinase sequence in their intracellular part, which is interrupted by a kinase insert domain, a transmembrane region and Impact of VEGF on PCs an extracellular part with seven immunoglobulin-like domains (Ferrara et al, 2003). Axitinib inhibits signal transduction mediated through the VEGFR-2 as well as VEGFR-1 and -3 (Kelly and Rixe, 2009)
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