Journal Article

Novel expression of sodium/<i>myo</i>-inositol co-transporter in podocytes in puromycin aminonucleoside nephrosis

Yusuke Watanabe, Tatsuya Kobayashi, Eishin Yaoita, Hiroshi Kawachi, Atsushi Yamauchi, Tsutomu Inoue, Fujio Shimizu, Yutaka Yoshida, Adel G. A. El-shemi, Hirokazu Okada, Hiromichi Suzuki and Tadashi Yamamoto

in Nephrology Dialysis Transplantation

Published on behalf of European Renal Association - European Dialysis and Transplant Assoc

Volume 19, issue 4, pages 817-822
Published in print April 2004 | ISSN: 0931-0509
Published online April 2004 | e-ISSN: 1460-2385 | DOI: http://dx.doi.org/10.1093/ndt/gfh026
Novel expression of sodium/myo-inositol co-transporter in podocytes in puromycin aminonucleoside nephrosis

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Background. How podocytes respond to injury is poorly understood, although podocyte injury in the glomerulus has been proposed as the crucial mechanism in the pathogenesis of proteinuria and focal segmental glomerulosclerosis. An increase in sodium/myo-inositol co-transporter (SMIT) transcripts, an osmoprotective gene, has been demonstrated in a variety of brain injury models. In the present study, we investigated SMIT expression in podocytes in experimental nephrosis.

Methods. Two types of nephrosis were induced in rats: puromycin aminonucleoside (PAN) nephrosis and monoclonal antibody (mAb) 5-1-6 nephropathy. Podocyte injury was morphologically distinct in the former type of nephrosis and limited to a minimum in the latter. SMIT expression in isolated glomeruli was estimated by ribonuclease protection assay. Localization of SMIT-expressing cells in glomeruli was examined by in situ hybridization.

Results. SMIT transcripts in glomeruli increased conspicuously in the nephrotic stage of PAN nephrosis, whereas the transcripts in cortices and medullae did not show significant changes. In situ hybridization revealed that podocytes were predominant cells expressing SMIT in the glomerulus. Significant increase of SMIT mRNA in the glomeruli was detected before the onset of massive proteinuria. In contrast, up-regulation of SMIT expression was not observed in mAb 5-1-6 nephropathy, whose urinary protein levels were comparable with those in the nephrotic stage of PAN nephrosis.

Conclusions. These findings suggest that SMIT expression in podocytes is not provoked by an effect of massive proteinuria but by extensive cellular injury.

Keywords: injury; monoclonal antibody 5-1-6; podocyte; puromycin aminonucleoside; sodium/myo-inositol co-transporter

Journal Article.  3701 words.  Illustrated.

Subjects: Nephrology

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