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Expression of intercellular adhesion molecule‐1 and vascular cell adhesion molecule‐1 in human crescentic glomerulonephritis
Author(s) -
Moon K C,
Park S Y,
Kim H W,
Hong H K,
Lee H S
Publication year - 2002
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1046/j.1365-2559.2002.01446.x
Subject(s) - vcam 1 , in situ hybridization , cell adhesion molecule , immunohistochemistry , intercellular adhesion molecule 1 , cytokeratin , pathology , glomerulonephritis , icam 1 , cell adhesion , biology , intercellular adhesion molecule , cd68 , microbiology and biotechnology , messenger rna , cell , medicine , kidney , endocrinology , gene , biochemistry
Expression of intercellular adhesion molecule‐1 and vascular cell adhesion molecule‐1 in human crescentic glomerulonephritis Aims:  In glomerulonephritis, intercellular adhesion molecule‐1 (ICAM‐1) and vascular cell adhesion molecule‐1 (VCAM‐1) may play important roles in the formation of crescents. These studies are designed to evaluate the expression patterns of ICAM‐1 and VCAM‐1 in human crescentic glomerulonephritis and to determine the cellular origin of adhesion molecules in the crescentic lesions. Methods and results:  We examined the expression of ICAM‐1 and VCAM‐1 proteins in renal biopsies with cellular ( n =7), fibrocellular ( n =9) or fibrous ( n =4) crescentic glomerulonephritis, and six controls by immunohistochemistry. mRNA expression of ICAM‐1 and VCAM‐1 was further evaluated by RNA in‐situ hybridization. Cytokeratin or CD68 immunohistochemistry was performed on the same sections, where in‐situ hybridization had been carried out. In cellular crescents, ICAM‐1 and VCAM‐1 proteins were over‐expressed to a similar extent. Of the three types of crescents, the extent of ICAM‐1 immunopositivity was the greatest in the cellular crescents and decreased towards the fibrous crescents ( P  < 0.05). Yet the extent of VCAM‐1 immunoreactivity was not different between the types. Fibrous crescents still contained some epithelial cells and showed only VCAM‐1 expression. In the glomeruli with cellular or fibrocellular crescents, the extent of ICAM‐1 immunopositivity in the glomerular tufts was significantly larger than that of VCAM‐1 ( P  < 0.05). In an in‐situ hybridization study, the mRNA expression patterns of ICAM‐1 and VCAM‐1 paralleled their protein expressions. A double‐labelling study showed that the signal for ICAM‐1 and VCAM‐1 mRNAs was mainly present in cytokeratin‐positive and CD68‐negative cells in the crescentic lesions. Conclusions:  These results suggest that glomerular parietal epithelial cells in cellular crescents up‐regulate both ICAM‐1 and VCAM‐1, and that some epithelial cells retained in fibrous crescents persistently over‐express VCAM‐1, but not ICAM‐1. They also suggest that ICAM‐1 is involved in early leucocyte recruitment into glomeruli in crescentic glomerulonephritis.

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