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Renal Expression of the Ets-1 Proto-oncogene during Progression of Rat Crescentic Glomerulonephritis

TAKASHI NAITO^*,, MOHAMMED S. RAZZAQUE^*, ARIFA NAZNEEN^*, DIANGE LIU^*, HIROSHI NIHEI, TAKEHIKO KOJI and TAKASHI TAGUCHI^*

^* Second Department of Pathology, Nagasaki University School of Medicine, Nagasaki, Japan
Department of Histology and Cell Biology, Nagasaki University School of Medicine, Nagasaki, Japan
Department of Medicine, Kidney Center, Tokyo Women's Medical College, Tokyo, Japan

Correspondence to Dr. Takashi Taguchi, Second Department of Pathology, Nagasaki University School of Medicine, 1-12-4, Sakamoto, Nagasaki 852-8523, Japan. Phone: 81-95-849-7055; Fax: 81-95-849-7056; E-mail: taguchi{at}net.nagasaki-u.ac.jp

Abstract. The ets-1 proto-oncogene is a member of the transcriptional factor family and was identified by homology to the v-ets oncogene. It was recently demonstrated that Ets-1 protein interacts with the promoter region of the genes coding for proteinases, including matrix metalloproteinase-1 (MMP-1), MMP-3, and urokinase-type plasminogen activator, suggesting that it may play an important role in the regulation of MMP expression. The role of the ets-1 proto-oncogene in advanced glomerular diseases, where extracellular matrix accumulation is observed, remains undefined. In this study, the expression of ets-1 mRNA and protein during the progression of rat crescentic glomerulonephritis was examined using immunohistochemical analysis, reverse transcription-PCR, and in situ hybridization. Passive accelerated anti-glomerular basement membrane-induced nephritis was induced in rats by intravenous injection of nephrotoxic serum. Rats were euthanized on day 7, 14, 21, 28, or 42. Immunohistochemical analysis demonstrated significant upregulation of Ets-1 protein expression in glomeruli and the interstitium in anti-glomerular basement membrane-induced nephritis. The numbers of Ets-1-positive cells were increased 8.8-fold on day 21 in glomeruli (1.2 ± 0.1 cells/glomerular cross-section, P < 0.001) and sixfold on day 28 in the interstitium (21 ± 1.3 cells/mm², P < 0.001), compared with control samples. Ets-1 protein was predominantly localized in glomerular epithelial cells, endothelial cells, and interstitial cells. A small number of vascular endothelial cells, macrophages, and T cells also expressed Ets-1 protein. MMP-3 deposition was upregulated and positive cells in the interstitium often coexpressed Ets-1, whereas only a few glomerular cells were positive for both MMP-3 and Ets-1 protein. The expression of ets-1 mRNA was also markedly increased in diseased kidneys. The distribution of ets-1 mRNA was similar to that of the protein. These results indicate that overexpression of the ets-1 proto-oncogene by phenotypically altered renal cells might be associated with the pathogenesis of rat crescentic glomerulonephritis.

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