Congenital vascular malformations - cerebral lesions differ from extracranial lesions by their immune expression of the glucose transporter protein GLUT1
Autor: | Allard C. van der Wal, Lorine B. Meijer-Jorna, Dirk Troost, Eleonora Aronica, Chris M. van der Loos |
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Přispěvatelé: | Other departments, ANS - Amsterdam Neuroscience, APH - Amsterdam Public Health, Neurology, Pathology, ACS - Amsterdam Cardiovascular Sciences |
Jazyk: | angličtina |
Rok vydání: | 2012 |
Předmět: |
CD31
Adult Intracranial Arteriovenous Malformations Male endocrine system Pathology medicine.medical_specialty Hemangioma Cavernous Central Nervous System Adolescent Pathology and Forensic Medicine Hemangioma Arteriovenous Malformations Medicine Humans Child Barrier function Glucose Transporter Type 1 biology business.industry Colocalization Soft tissue General Medicine medicine.disease Molecular biology Immunohistochemistry carbohydrates (lipids) Neurology biology.protein Choroid plexus GLUT1 Female Neurology (clinical) business |
Zdroj: | Clinical neuropathology, 31(3), 135-141. Dustri-Verlag Dr. Karl Feistle |
ISSN: | 0722-5091 |
Popis: | 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. |
Databáze: | OpenAIRE |
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