title: Downregulated expression of ADAM9 in anterior polar cataracts.
abstract: OBJECTIVE
  To determine whether ADAM (a disintegrin and metalloproteinase) is regulated in lens epithelial cells (LECs) of patients with anterior polar cataracts and by transforming growth factor (TGF)-beta 1 in cultured LECs.
  
  
  METHODS
  Department of Ophthalmology and Visual Science, College of Medicine, The Catholic University of Korea, Seoul, Korea.
  
  
  METHODS
  Lens epithelial cells attached to the anterior capsules of human cataractous lenses with nuclear and anterior subcapsular cataracts and noncataractous lenses were analyzed by reverse transcribed-polymerase chain reaction for the expression of ADAMs. The effect of TGF-beta 1 on ADAM gene expression was also tested in mouse lens epithelial explants and cultured LEC lines (alpha TN-4 and HLE B-3).
  
  
  RESULTS
  Significantly reduced expression of mRNA for ADAM9 was observed in LECs from patients with anterior polar cataracts. The expression of mRNA for ADAM9 was downregulated by TGF-beta 1 in cultured human LECs. Treatment of cultured mouse LECs with TGF-beta 1 led to a reduction in ADAM1 mRNA.
  
  
  CONCLUSIONS
  ADAMs are expressed and regulated in LECs. The downregulated expression of ADAM9 may serve as a marker for anterior polar cataracts in addition to previously known proteins, fibronectin, alpha-SMA, and beta ig-h3. The functions of this protein in lens pathology require further investigation.
authors.affiliation: Laboratory of Ophthalmology and Visual Science, College of Medicine, The Catholic University of Korea and Catholic Research Institutes of Medical Sciences, Seoul, South Korea.
authors.forename: Jung Min
authors.initials: JM
authors.lastname: Lim
authors.forename: Jin-Hak
authors.initials: JH
authors.lastname: Lee
authors.forename: Won-Ryang
authors.initials: WR
authors.lastname: Wee
authors.forename: Choun-Ki
authors.initials: CK
authors.lastname: Joo
mesh_terms: D051722:ADAM Proteins; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000818:Animals; D015415:Biomarkers; D002386:Cataract / Q000235:genetics* / Q000378:metabolism; D002460:Cell Line; D019483:Disintegrins / Q000235:genetics* / Q000378:metabolism; D015536:Down-Regulation; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism; D005136:Eye Proteins / Q000235:genetics* / Q000378:metabolism; D000072196:Fertilins; D015870:Gene Expression; D006801:Humans; D007908:Lens, Crystalline / Q000166:cytology; D008562:Membrane Glycoproteins / Q000378:metabolism; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism; D008666:Metalloendopeptidases / Q000235:genetics* / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D008875:Middle Aged; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D016212:Transforming Growth Factor beta / Q000494:pharmacology; D053773:Transforming Growth Factor beta1
chemical_list: D015415:Biomarkers; D019483:Disintegrins; D005136:Eye Proteins; D008562:Membrane Glycoproteins; D008565:Membrane Proteins; D012333:RNA, Messenger; C508960:TGFB1 protein, human; C508961:Tgfb1 protein, mouse; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; D051722:ADAM Proteins; C098339:ADAM9 protein, human; C498316:Adam9 protein, mouse; D000072196:Fertilins; D008666:Metalloendopeptidases