title: Up-regulation of TRAIL mRNA expression in peripheral blood mononuclear cells from patients with minimal-change nephrotic syndrome.
abstract: BACKGROUND
  Minimal-change nephrotic syndrome (MCNS) is considered to be associated with T-cell dysfunction and with the abnormal secretion of putative glomerular permeability factors; however, the nature of such factors remains elusive.
  
  
  METHODS
  To identify up-regulated genes during the nephrosis phase, we undertook serial analyses of gene expression (SAGE) in peripheral blood mononuclear cells (PBMC) from a patient with MCNS sampled during the nephrosis and remission phases. To confirm the SAGE results, we performed quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR) analyses. We also measured the serum levels of the identified gene product in nephrosis and remission samples from 29 MCNS patients, 57 patients with nephrotic syndrome due to other types of glomerular diseases and 30 healthy individuals.
  
  
  RESULTS
  Using more than 20,000 SAGE tags, we identified 15 functionally known genes that were up-regulated (>or=4-fold) in PBMC from the MCNS patient during the nephrosis phase. For further examination, we selected two genes encoding secretory proteins, namely tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) and tissue inhibitor of metalloprotease 1. Real-time RT-PCR analysis confirmed a higher expression of TRAIL mRNA in PBMC during nephrosis than during remission in eight MCNS patients. The expression pattern of TRAIL mRNA, however, was variable among four patients with membranous nephropathy. There was no significant increase of serum levels of a soluble form of TRAIL in MCNS patients during the nephrosis phase.
  
  
  CONCLUSIONS
  These results suggest that the intracellular TRAIL mRNA expression in PBMC is up-regulated in MCNS patients during the nephrosis phase. This change may represent either an epiphenomenon or it may provide a potential explanation for the altered T-cell function in MCNS.
authors.affiliation: Third Department of Internal Medicine, Akita University School of Medicine, 1-1-1 Hondo, Akita City, Akita 010-8543, Japan.
authors.forename: Shin
authors.initials: S
authors.lastname: Okuyama
authors.forename: Atsushi
authors.initials: A
authors.lastname: Komatsuda
authors.forename: Hideki
authors.initials: H
authors.lastname: Wakui
authors.forename: Namiko
authors.initials: N
authors.lastname: Aiba
authors.forename: Naohito
authors.initials: N
authors.lastname: Fujishima
authors.forename: Keiko
authors.initials: K
authors.lastname: Iwamoto
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ohtani
authors.forename: Ken-ichi
authors.initials: K
authors.lastname: Sawada
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D051017:Apoptosis Regulatory Proteins; D016022:Case-Control Studies; D005260:Female; D020869:Gene Expression Profiling; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000378:metabolism*; D008297:Male; D008562:Membrane Glycoproteins / Q000235:genetics* / Q000378:metabolism*; D008875:Middle Aged; D009402:Nephrosis, Lipoid / Q000235:genetics* / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D012075:Remission, Spontaneous; D053221:TNF-Related Apoptosis-Inducing Ligand; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000235:genetics / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics* / Q000378:metabolism*; D015854:Up-Regulation / Q000235:genetics*
chemical_list: D051017:Apoptosis Regulatory Proteins; D008562:Membrane Glycoproteins; D012333:RNA, Messenger; D053221:TNF-Related Apoptosis-Inducing Ligand; C505653:TNFSF10 protein, human; D019715:Tissue Inhibitor of Metalloproteinase-1; D014409:Tumor Necrosis Factor-alpha