title: Serum from minimal change patients in relapse increases CD80 expression in cultured podocytes.
abstract: BACKGROUND
  Minimal change disease (MCD) is the most common cause of nephrotic syndrome in children and is associated with the expression of CD80 in podocytes and the increased excretion of CD80 in urine. We hypothesized that serum from patients with MCD might stimulate CD80 expression in cultured podocytes.
  
  
  METHODS
  Sera and peripheral blood mononuclear cells (PBMCs) were collected from subjects with MCD in relapse and remission and from normal controls. Immortalized human podocytes were incubated with culture media containing patient sera or supernatants from patient and control PBMC cultures. CD80 expression was measured by quantitative PCR and western blot analysis.
  
  
  RESULTS
  Sera collected from patients with MCD in relapse, but not in remission, significantly increased CD80 expression (mean ± standard deviation: 1.8 ± 0.7 vs. 0.8 ± 0.2; p < 0.004) and CD80 protein secretion by podocytes (p < 0.05 between relapse and normal controls). No such CD80 increase was observed when podocytes were incubated with supernatants of PBMC cultures from patients in relapse.
  
  
  CONCLUSIONS
  Sera from MCD patients in relapse, but not in remission, stimulated CD80 expression in cultured podocytes. Identifying this factor in sera could provide insights into the pathogenesis of this disorder. No role in CD80 expression by podocytes was found for cytokines released by PBMCs.
authors.affiliation: Division of Renal Diseases and Hypertension, Department of Medicine, University of Colorado, Denver, CO, USA.
authors.forename: Takuji
authors.initials: T
authors.lastname: Ishimoto
authors.forename: Gabriel
authors.initials: G
authors.lastname: Cara-Fuentes
authors.forename: Heiman
authors.initials: H
authors.lastname: Wang
authors.forename: Michiko
authors.initials: M
authors.lastname: Shimada
authors.forename: Clive H
authors.initials: CH
authors.lastname: Wasserfall
authors.forename: William E
authors.initials: WE
authors.lastname: Winter
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: Rivard
authors.forename: Carlos E
authors.initials: CE
authors.lastname: Araya
authors.forename: Moin A
authors.initials: MA
authors.lastname: Saleem
authors.forename: Peter W
authors.initials: PW
authors.lastname: Mathieson
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Johnson
authors.forename: Eduardo H
authors.initials: EH
authors.lastname: Garin
mesh_terms: D000293:Adolescent; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D018122:B7-1 Antigen / Q000096:biosynthesis*; D015153:Blotting, Western; D002478:Cells, Cultured; D002648:Child; D002675:Child, Preschool; D016207:Cytokines / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D024601:Glyceraldehyde 3-Phosphate Dehydrogenase (NADP+) / Q000378:metabolism; D006801:Humans; D007677:Kidney Function Tests; D008297:Male; D009000:Monocytes / Q000378:metabolism; D009402:Nephrosis, Lipoid / Q000097:blood / Q000188:drug therapy / Q000378:metabolism*; D050199:Podocytes / Q000378:metabolism*; D011241:Prednisone / Q000627:therapeutic use; D012313:RNA / Q000096:biosynthesis / Q000235:genetics / Q000302:isolation & purification; D060888:Real-Time Polymerase Chain Reaction; D012008:Recurrence; D044967:Serum; D055815:Young Adult
chemical_list: D000893:Anti-Inflammatory Agents; D018122:B7-1 Antigen; D016207:Cytokines; D012313:RNA; D024601:Glyceraldehyde 3-Phosphate Dehydrogenase (NADP+); D011241:Prednisone