title: TGF-beta-induced apoptosis and reduction of Bcl-2 in human lens epithelial cells in vitro.
abstract: OBJECTIVE
  TGF-beta has been shown to induce lens epithelial cells to undergo an aberrant growth and transdifferentiation that mimic some characteristics of anterior subcapsular cataract, and posterior capsular opacification. Here we sought to examine whether TGF-beta induces apoptotic cell death in human lens epithelial cells in vitro.
  
  
  METHODS
  Cell death of human lens epithelial cells HLE-B3 cell line was measured by TUNEL assay, FACS analysis, and DNA fragmentation assay. The expression of Bcl-2 and Bax was examined using reverse transcription-polymerase chain reaction and Western blot analysis. The expression of poly (ADP-ribose) polymerase (PARP) and caspase-3 was examined using Western blot analysis.
  
  
  RESULTS
  TGF-beta-induced cell death was detected in human lens epithelial cells by TUNEL assay. DNA fragmentation assay showed the characteristic laddering pattern from the genomic DNA from human lens epithelial cells treated with TGF-beta. The expression of Bcl-2 mRNA and its protein was markedly decreased in human lens epithelial cells treated with TGF-beta. Caspase-3 and PARP were not activated in this process.
  
  
  CONCLUSIONS
  This study suggests that TGF-beta induces apoptotic cell death in human lens epithelial cells and that decreased expression of Bcl-2 might play a role in this process.
authors.affiliation: Department of Ophthalmology, Institute of Vision Research, Yonsei University College of Medicine, Seoul, Korea.
authors.forename: Joon H
authors.initials: JH
authors.lastname: Lee
authors.forename: Xiu Hua
authors.initials: XH
authors.lastname: Wan
authors.forename: Jeongmin
authors.initials: J
authors.lastname: Song
authors.forename: Jimmy Jaeyoung
authors.initials: JJ
authors.lastname: Kang
authors.forename: Woo-Sook
authors.initials: WS
authors.lastname: Chung
authors.forename: Eunjoo H
authors.initials: EH
authors.lastname: Lee
authors.forename: Eung Kweon
authors.initials: EK
authors.lastname: Kim
mesh_terms: D017209:Apoptosis / Q000187:drug effects*; D015153:Blotting, Western; D053148:Caspase 3; D020169:Caspases / Q000378:metabolism; D002478:Cells, Cultured; D004247:DNA / Q000032:analysis; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D005434:Flow Cytometry; D019254:Genes, bcl-2 / Q000235:genetics; D006801:Humans; D007166:Immunosuppressive Agents / Q000494:pharmacology*; D020287:In Situ Nick-End Labeling; D007908:Lens, Crystalline / Q000166:cytology*; D011065:Poly(ADP-ribose) Polymerases / Q000378:metabolism; D011518:Proto-Oncogene Proteins / Q000235:genetics / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D016212:Transforming Growth Factor beta / Q000494:pharmacology*; D053781:Transforming Growth Factor beta2; D051028:bcl-2-Associated X Protein
chemical_list: C494826:BAX protein, human; D007166:Immunosuppressive Agents; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D012333:RNA, Messenger; C509041:TGFB2 protein, human; D016212:Transforming Growth Factor beta; D053781:Transforming Growth Factor beta2; D051028:bcl-2-Associated X Protein; D004247:DNA; D011065:Poly(ADP-ribose) Polymerases; C505407:CASP3 protein, human; D053148:Caspase 3; D020169:Caspases