title: [Apoptosis of human umbilical vein endothelial cells induced by IgA1 isolated from Henoch-Schönlein purpura patients].
abstract: OBJECTIVE
  To observe the effect of apoptosis of human umbilical vein endothelial cells (HUVEC) induced by IgA1 from Henoch-Schönlein purpura (HSP) patients.
  
  
  METHODS
  HUVEC were cultured in 3 different conditional media with IgA1 from HSP patients, normal healthy children and simply the cell culture medium. Serum IgA1 was purified by jacalin affinity chromatography, rates of apoptosis in HUVEC cells at different concentration and different times after incubation with IgA1 were determined by TUNEL method and flow cytometry. Real-time PCR and Western blot methods were used to detect the expression of caspase-3 and Fas, respectively.
  
  
  RESULTS
  Apoptosis rate of HUVEC by IgA1 isolated from HSP patients were significantly higher than that of the blank control [(14.77 ± 2.23)% vs. (2.25 ± 0.77)%, P < 0.01] and the apoptosis rate of HUVEC induced by IgA1 from normal healthy children was higher than that of blank control [(7.97 ± 1.48)% vs. (2.25 ± 0.77)%, P < 0.01]. The apoptosis rate of HUVEC induced by IgA1 from HSP was time and concentration-dependent. Moreover IgA1 isolated from HSP patients could significantly increase the caspase-3 and Fas expression (P < 0.01).
  
  
  CONCLUSIONS
  The IgA1 from HSP patients could induce the apoptosis of HUVEC, which might be related to the progression of HSP.
authors.affiliation: Department of Pediatrics, First Affiliated Hospital of Anhui Medical University, Hefei, China.
authors.forename: Wen-jun
authors.initials: WJ
authors.lastname: Fei
authors.forename: Bo
authors.initials: B
authors.lastname: Yan
authors.forename: Li-ping
authors.initials: LP
authors.lastname: Yuan
authors.forename: Qin
authors.initials: Q
authors.lastname: Zhang
authors.forename: Bo
authors.initials: B
authors.lastname: Hu
authors.forename: Ling
authors.initials: L
authors.lastname: Lu
mesh_terms: D000293:Adolescent; D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3 / Q000235:genetics / Q000378:metabolism; D002478:Cells, Cultured; D002648:Child; D002675:Child, Preschool; D004305:Dose-Response Relationship, Drug; D053222:Fas Ligand Protein / Q000235:genetics / Q000378:metabolism; D005260:Female; D005434:Flow Cytometry; D005786:Gene Expression Regulation / Q000187:drug effects; D061307:Human Umbilical Vein Endothelial Cells / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D006801:Humans; D011695:IgA Vasculitis / Q000097:blood* / Q000276:immunology; D007070:Immunoglobulin A / Q000097:blood / Q000302:isolation & purification / Q000494:pharmacology*; D020287:In Situ Nick-End Labeling; D008297:Male; D012333:RNA, Messenger / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction; D013997:Time Factors
chemical_list: C505661:FASLG protein, human; D053222:Fas Ligand Protein; D007070:Immunoglobulin A; D012333:RNA, Messenger; C505407:CASP3 protein, human; D053148:Caspase 3