title: Expression of Zonulin, c-kit, and Glial Fibrillary Acidic Protein in Human Gliomas.
abstract: The hallmarks of human malignant gliomas are their marked invasiveness and vascularity. Because angiogenesis and tumor invasion have been associated with extracellular matrix degradation and intercellular tight junctions, the involvement of zonulin in glioma biology is in the focus. We selected for histological examination five cases of glioblastoma WHO IV (nomenclature of the World Health Organization) and one case each from astrocytoma WHO III, meningioma WHO III, and meningioma WHO I as control samples. The meningioma WHO I is regarded as benign, whereas the meningioma WHO III is recognized as the transition form of malignant tumors in humans. The visualization of a newly designed antibody against human zonulin was studied in triple-labeling studies using fluorescence immunocytochemistry and compared with the expression of c-kit and glial fibrillary acidic protein in differently developed human gliomas. We found that increasing the expression of c-kit is accompanied by an increase of zonulin expression. Both are correlated to the degree of malignancy of human brain tumors. The expression of zonulin is correlated to the degradation of the blood-brain barrier as revealed by Griffonia simplicifolia lectin. In differently graded tumors, we found differently graded involvement of blood vessels in the tumor development, explaining patients' survival.
authors.affiliation: Department of Neurosurgery, University Hospital, Liebigstr. 20, D-04103 Leipzig, Germany.
authors.forename: Marco
authors.initials: M
authors.lastname: Skardelly
authors.forename: Franz Paul
authors.initials: FP
authors.lastname: Armbruster
authors.forename: Jürgen
authors.initials: J
authors.lastname: Meixensberger
authors.forename: Heidegard
authors.initials: H
authors.lastname: Hilbig
references.citation: J Cell Sci. 2000 Dec;113 Pt 24:4435-40
references.pmid: 11082037
references.citation: Gut. 2003 Feb;52(2):218-23
references.pmid: 12524403
references.citation: J Neurooncol. 2005 Nov;75(2):195-202
references.pmid: 16132504
references.citation: Infect Immun. 2003 Apr;71(4):1897-902
references.pmid: 12654806
references.citation: J Pathol. 2007 Mar;211(4):481-8
references.pmid: 17294421
references.citation: J Neurooncol. 2005 Nov;75(2):163-7
references.pmid: 16132509
references.citation: J Clin Invest. 1989 Apr;83(4):1089-94
references.pmid: 2649511
references.citation: Gastroenterology. 2002 Nov;123(5):1607-15
references.pmid: 12404235
references.citation: J Neurooncol. 2006 Jan;76(2):105-9
references.pmid: 16205964
references.citation: Ann N Y Acad Sci. 2000;915:214-22
references.pmid: 11193578
references.citation: J Clin Invest. 1989 Feb;83(2):724-7
references.pmid: 2492310
references.citation: Scand J Gastroenterol. 2006 Apr;41(4):408-19
references.pmid: 16635908
references.citation: J Biol Chem. 2001 Jun 1;276(22):19160-5
references.pmid: 11278543
references.citation: Clin Neuropathol. 2006 May-Jun;25(3):107-14
references.pmid: 16719406
references.citation: Curr Opin Gastroenterol. 2008 Nov;24(6):687-91
references.pmid: 19122516
references.citation: Cancer Cell. 2006 Apr;9(4):287-300
references.pmid: 16616334