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  • 1
    ISSN: 1432-0533
    Keywords: Key words Vascular endothelial growth factor ; Brain tumor ; Astrocytoma ; Angiogenesis ; Vascularization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Marked neovascularization is a hallmark of many neoplasms in the nervous system. Recent reports indicate that the endothelial mitogen vascular endothelial growth factor (VEGF) may play a critical role in the regulation of vascular endothelial proliferation in malignant gliomas. Using novel monoclonal antibodies to the VEGF polypeptide we have determined the expression and cellular distribution of VEGF protein in a representative series of 171 human central nervous system (CNS) tumors by immunohistochemistry and immunoblotting. In agreement with previous in situ hybridization data, 19 out of 20 glioblastomas (95%) showed immunoreactivity for VEGF, whereas both the percentage of immunoreactive tumors and the extent of immunoreactivity for VEGF were significantly lower in astrocytomas. Of the pilocytic astrocytomas (WHO grade I) 44% were immunoreactive for VEGF, but we observed several cases with pronounced vascular proliferates in the absence of VEGF. In ependymomas, meningiomas, hemangioblastomas, and primitive neuroectodermal tumors, there was no correlation between VEGF expression, vascular endothelial proliferation and the grade of malignancy. Oligodendrogliomas and the oligodendroglial component of mixed gliomas lacked immunoreactive VEGF, indicating that endothelial growth factors other than VEGF may regulate tumor angiogenesis in these neoplasms. Western blot analysis showed a predominant VEGF protein species of 23 kDa and confirmed the immunohistochemical data in all cases. Our findings demonstrate that VEGF is expressed in a wide spectrum of brain tumors in which it may induce neovascularization. However, other angiogenic factors also appear to contribute to the vascularization of CNS neoplasms.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    The journal of membrane biology 143 (1995), S. 29-35 
    ISSN: 1432-1424
    Keywords: Na+-K+-ATPase ; Electrophysiology ; K+ channel ; Tetraethylammonium ; Conductance regulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract Using the two-microelectrode voltage clamp technique in Xenopus laevis oocytes, we estimated Na+-K+-ATPase activity from the dihydroouabain-sensitive current (I DHO) in the presence of increasing concentrations of tetraethylammonium (TEA+; 0, 5, 10, 20, 40 mm), a well-known blocker of K+ channels. The effects of TEA+ on the total oocyte currents could be separated into two distinct parts: generation of a nonsaturating inward current increasing with negative membrane potentials (V M) and a saturable inhibitory component affecting an outward current easily detectable at positive V M. The nonsaturating component appears to be a barium-sensitive electrodiffusion of TEA+ which can be described by the Goldman-Hodgkin-Katz equation, while the saturating component is consistent with the expected blocking effect of TEA+ on K+ channels. Interestingly, this latter component disappears when the Na+-K+-ATPase is inhibited by 10 μm DHO. Conversely, TEA+ inhibits a component of I DHO with a k d of 25±4 mm at +50 mV. As the TEA+-sensitive current present in I DHO reversed at −75 mV, we hypothesized that it could come from an inhibition of K+ channels whose activity varies in parallel with the Na+-K+-ATPase activity. Supporting this hypothesis, the inward portion of this TEA+-sensitive current can be completely abolished by the addition of 1 mm Ba2+ to the bath. This study suggests that, in X. laevis oocytes, a close link exists between the Na-K-ATPase activity and TEA+-sensitive K+ currents and indicates that, in the absence of effective K+ channel inhibitors, I DHO does not exclusively represent the Na+-K+-ATPase-generated current.
    Type of Medium: Electronic Resource
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