Platelet endothelial cell adhesion molecule-1 and angiogenic factor expression in idiopathic membranous nephropathy.
BACKGROUND
Idiopathic membranous nephropathy (IMN), a principal disease of glomerular capillaries, was investigated for some aspects of glomerular capillary injury and repair (angiogenesis).


METHODS
Fifteen cases of IMN were studied immunohistochemically for expression of the endothelial cell antigen platelet endothelial cell adhesion molecule-1 (PECAM-1[CD31]) and the angiogenesis-stimulating factors vascular endothelial growth factor (VEGF) and thymidine phosphorylase (TP). An equal number of normal control kidneys of fetal and mature origin were tested for the same antigens.


RESULTS
Normal tissues expressed PECAM-1 in both glomerular and interstitial endothelial cells, whereas VEGF and TP were expressed in the tubular epithelium. IMN was characterized by complete or partial loss of PECAM-1 expression from glomerular capillaries and a parallel gain/expression of this antigen by the tubular epithelium. In addition, VEGF and TP expression was lost or considerably reduced from tubular cells of IMN.


CONCLUSIONS
We hypothesize that PECAM-1 expression by tubular epithelial cells represents uptake of CD31(+) cell-surface fragments released by glomerular endothelial cells after glomerular damage. The damage is confounded by the failure of angiogenic mechanisms to promote glomerular angiogenesis (repair) because both VEGF and TP stimulation by the tubular epithelium is eliminated. It is suggested that immunohistochemical detection of VEGF or TP in the tubular epithelium may be useful in understanding the pathogenesis of IMN.
Sivridis
Efthimios
E
Departments of Pathology and Nephrology, Democritus University of Thrace, Alexandroupolis, Greece.
Giatromanolaki
Alexandra
A
Touloupidis
Stavros
S
Pasadakis
Ploumis
P
Vargemezis
Vasilios
V
D000368:Aged; D043925:Angiogenesis Inducing Agents / Q000096:biosynthesis* / Q000276:immunology; D016228:Endothelial Growth Factors / Q000096:biosynthesis / Q000276:immunology; D004730:Endothelium, Vascular / Q000737:chemistry / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology; D005260:Female; D005333:Fetus / Q000098:blood supply / Q000737:chemistry / Q000201:enzymology / Q000473:pathology; D015433:Glomerulonephritis, Membranous / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D007150:Immunohistochemistry; D036341:Intercellular Signaling Peptides and Proteins / Q000096:biosynthesis / Q000276:immunology; D007678:Kidney Glomerulus / Q000098:blood supply / Q000737:chemistry / Q000196:embryology / Q000473:pathology; D007684:Kidney Tubules / Q000098:blood supply / Q000737:chemistry / Q000201:enzymology / Q000473:pathology; D008222:Lymphokines / Q000096:biosynthesis / Q000276:immunology; D008297:Male; D008875:Middle Aged; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000096:biosynthesis* / Q000276:immunology; D013939:Thymidine Phosphorylase / Q000096:biosynthesis / Q000276:immunology; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors
D043925:Angiogenesis Inducing Agents; D016228:Endothelial Growth Factors; D036341:Intercellular Signaling Peptides and Proteins; D008222:Lymphokines; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors; D013939:Thymidine Phosphorylase