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Alkmaar, Netherlands

Cerebral vascular malformations were investigated for the presence of the glucose transporter protein GLUT1, which is normally expressed in endothelial cells of the pre-existing microvasculature of the brain and absent in the vasculature of the choroid plexus and extracranial vasculature without a barrier function. Extracranial arteriovenous malformations (AVM) are known to show an absence of GLUT1 expression which distinguishes them from infantile hemangioma of skin and soft tissue. The expression of GLUT1 in cerebrovascular malformations is not systematically investigated. Paraffin-embedded sections of cerebral AVM (4), including one choroid plexus AVM, cerebral cavernous malformations (CCM, 3) and extracranial (facial) AVM (3) were immunostained with anti-CD31 and GLUT1 in doublestaining procedure which was further analyzed with the use of spectral analysis software. All 7 cases of cerebral vascular malformations showed colocalization of GLUT1/CD31 of endothelial cells of the vessels within the malformation. Only in the extracranial AVM expression of GLUT1 was completely absent. Cerebral AVM differ from extracranial AVM by their endothelial immunoexpression of GLUT1, indicating that the vessels of these malformations retain the endothelial phenotype of the local vascular beds from which they are derived during embryogenesis. Source


Background: Cerebral vascular malformations were investigated for the presence of the glucose transporter protein GLUT1, which is normally expressed in endothelial cells of the pre-existing microvasculature of the brain and absent in the vasculature of the choroid plexus and extracranial vasculature without a barrier function. Extracranial arteriovenous malformations (AVM) are known to show an absence of GLUT1 expression which distinguishes them from infantile hemangioma of skin and soft tissue. The expression of GLUT1 in cerebrovascular malformations is not systematically investigated. Methods: Paraffin-embedded sections of cerebral AVM (4), including one choroid plexus AVM, cerebral cavernous malformations (CCM, 3) and extracranial (facial) AVM (3) were immunostained with anti-CD31 and GLUT1 in doublestaining procedure which was further analyzed with the use of spectral analysis software. Results: All 7 cases of cerebral vascular malformations showed colocalization of GLUT1/CD31 of endothelial cells of the vessels within the malformation. Only in the extracranial AVM expression of GLUT1 was completely absent. Conclusion: Cerebral AVM differ from extracranial AVM by their endothelial immunoexpression of GLUT1, indicating that the vessels of these malformations retain the endothelial phenotype of the local vascular beds from which they are derived during embryogenesis©2012 Dustri-Verlag Dr. K. Feistle ISSN 0722-5091. Source


Meijer-Jorna L.B.,Symbiant Medical Center Alkmaar | Van Der Loos C.M.,University of Amsterdam | Teeling P.,University of Amsterdam | De Boer O.J.,University of Amsterdam | And 3 more authors.
Journal of Cutaneous Pathology | Year: 2012

Background: Areas of microvascular proliferation have been observed in a subpopulation of symptomatic congenital vascular malformations later in life. We investigated whether this angiogenic response is followed by a stage of maturation. Methods: Resections of vascular malformations (n = 15), infantile hemangiomas (IHs) (n = 8) and pyogenic granulomas (PGs) (n = 5) were studied. Histopathologically, all lesions were screened for presence of foci of immature and/or mature microvessels. These areas were further studied immunohistochemically for differential expression of several angiogenic factors, cell cycle-dependent proteins, p53 and active caspase3. Immunostains were scored semiquantitatively. Results: Immature microvessel areas were present in five vascular malformations (all of the arteriovenous type), five IHs and five PGs; these lesions also contained transitions between immature and mature microvessels. Conglomerates of mature microvessels were found in 19 cases (6 vascular malformations, 5 PGs and 8 IHs). Expression of vascular endothelial growth factor-A, angiopoietin-1, Ki-67, p16 and p21/27 ratios were overall significantly lower in mature areas than in immature areas including those in vascular malformations. P53 and caspase3 expression was scarce in all lesions. Conclusions: Microvascular areas in vascular malformations appear to follow the same pattern of vascular proliferation and maturation as seen in other microvascular lesions of skin and soft tissue. Copyright © 2012 John Wiley & Sons A/S. Source

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