In:
Archives of Pathology & Laboratory Medicine, Archives of Pathology and Laboratory Medicine, Vol. 134, No. 12 ( 2010-12-01), p. 1804-1812
Kurzfassung:
Context—Plasminogen kringle domain (K) 5 is known to inhibit endothelial cell growth, but limited data are available investigating the relationship between K5 and glomerulonephritis (GN). Objective—To understand the relationships among K5, GN, and glomerular endothelial cells in GN mice models and human subjects. Design—Two mice models of GN and 2 categories of human GN biopsy samples were collected to gain insight into the disease mechanism from the laboratory to bedside. In the mechanistic animal study, membranous nephropathy (MN) and focal segmental glomerulosclerosis mice models were used. Kringle domain 5 in the diseased kidney was located by immunofluorescence and quantified by Western blotting. In the kinetic animal study, different MN time points were stained with K5, immunoglobulin G, and C3 by immunofluorescence. CD31 and proliferating cell nuclear antigen were evaluated by immunohistochemical double staining for alterations in the glomerular endothelial cells. Biopsy samples from patients diagnosed with antibody (Ab)-mediated and non-Ab–mediated GN were collected for K5 analysis. Results—The expression level of K5 was found to be significant in MN, but not in focal segmental glomerulosclerosis, and was markedly elevated in the diseased glomeruli along the capillary walls. Kringle domain 5 levels increased steadily with the evolution of MN, appearing after the deposition of Abs. In altered glomerular endothelial cells, CD31 decreased with the evolution of MN. In human subjects, K5 occurred only in patients with Ab GN. Conclusions—Kringle domain 5 might be involved in the progression of Ab-mediated GN and associated with the alteration of MN glomerular endothelial cell growth.
Materialart:
Online-Ressource
ISSN:
1543-2165
,
0003-9985
DOI:
10.5858/2009-0490-OAR.1
Sprache:
Englisch
Verlag:
Archives of Pathology and Laboratory Medicine
Publikationsdatum:
2010
ZDB Id:
2028916-9
