title: Novel expression of sodium/myo-inositol co-transporter in podocytes in puromycin aminonucleoside nephrosis.
abstract: 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.
authors.affiliation: Department of Structural Pathology, Institute of Nephrology, Graduate School of Medical and Dental Sciences, Niigata University, 1-757 Asahimachi-dori, Niigata, 951-8510, Japan.
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Watanabe
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Kobayashi
authors.forename: Eishin
authors.initials: E
authors.lastname: Yaoita
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kawachi
authors.forename: Atsushi
authors.initials: A
authors.lastname: Yamauchi
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Inoue
authors.forename: Fujio
authors.initials: F
authors.lastname: Shimizu
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Yoshida
authors.forename: Adel G A
authors.initials: AG
authors.lastname: El-Shemi
authors.forename: Hirokazu
authors.initials: H
authors.lastname: Okada
authors.forename: Hiromichi
authors.initials: H
authors.lastname: Suzuki
authors.forename: Tadashi
authors.initials: T
authors.lastname: Yamamoto
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000008:administration & dosage; D006360:Heat-Shock Proteins / Q000096:biosynthesis*; D007678:Kidney Glomerulus / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D008565:Membrane Proteins / Q000096:biosynthesis*; D009401:Nephrosis / Q000378:metabolism*; D011692:Puromycin Aminonucleoside / Q000008:administration & dosage; D051381:Rats; D011921:Rats, Inbred WKY; D027981:Symporters / Q000096:biosynthesis*; D019459:Urothelium / Q000166:cytology* / Q000378:metabolism*
chemical_list: D000911:Antibodies, Monoclonal; D006360:Heat-Shock Proteins; D008565:Membrane Proteins; D027981:Symporters; C073884:SLC5A3 protein, human; D011692:Puromycin Aminonucleoside