Nephrol Dial Transplant (2004) 19: 817-822
Nephrol Dial Transplant Vol. 19 No. 4 © ERA-EDTA 2004; all rights reserved
Original Article
Novel expression of sodium/myo-inositol co-transporter in podocytes in puromycin aminonucleoside nephrosis
1Department of Structural Pathology and 2Department of Cell Biology, Institute of Nephrology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, 3Department of Nephrology, Saitama Medical School, Saitama and 4Division of Nephrology, Department of Medicine, Osaka Rosai Hospital, Osaka, Japan
Correspondence and offprint requests to: Eishin Yaoita, Department of Structural Pathology, Institute of Nephrology, Graduate School of Medical and Dental Sciences, Niigata University, 1-757 Asahimachi-dori, Niigata, 951-8510, Japan. Email: ren-path{at}med.niigata-u.ac.jp Y. Watanabe and T. Kobayashi contributed equally to this work.
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
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  L. Zhao, E. Yaoita, M. Nameta, Y. Zhang, L. M. Cuellar, H. Fujinaka, B. Xu, Y. Yoshida, K. Hatakeyama, and T. Yamamoto Claudin-6 localized in tight junctions of rat podocytes Am J Physiol Regulatory Integrative Comp Physiol, June 1, 2008; 294(6): R1856 - R1862. [Abstract] [Full Text] [PDF]
|
|