title: Human idiopathic epiretinal membranes express NGF and NGF receptors.
abstract: OBJECTIVE
  Glial cells and fibroblasts (FBs) play a key role in epiretinal membrane (ERM) development and progression. Myofibroblasts (myoFBs), arising from these cells, can lead to the hypertrophic scars and tissue contraction observed in ERMs. Nerve growth factor (NGF) and transforming growth factor-beta1 (TGF-beta1) play a crucial role in FB activities. Therefore, the authors evaluated myoFBs in ERMs and NGF, trkA(NGFR and p75(NTR) expression, as well as TGF-beta1/TGF-betaRII levels in both ERMs and vitreous.
  
  
  METHODS
  Eight idiopathic ERMs and vitreous were obtained from patients at the time of vitrectomy for macular pucker. Ten control vitreous were from donors. Biochemical and molecular analyses were performed to identify alpha-smooth muscle actin (alpha-SMA, a defined myoFB marker), NGF, trkA(NGFR)/p75(NTR), and TGF-beta1/TGF-betaRII.
  
  
  RESULTS
  Every idiopathic ERM displayed alpha-SMA positive myoFBs, expressing NGF, trkA(NGFR), and p75(NTR). ERM vitreous showed a significant decrease in NGF protein coupled with a TGF-beta1 increase. In addition, vitreous cells showed an increase in trkA(NGFR)/p75(NTR) mRNA associated with a decrease in TGF-betaRII mRNA.
  
  
  CONCLUSIONS
  Idiopathic ERMs were characterized by myoFBs. The expression of NGF, trkA, and p75 in local myoFBs associated with changes in ERM vitreous NGF suggests an involvement of NGF, as previously reported for TGF-beta1, in the evolution and myoFB-mediated contractile activity of ERMs.
authors.affiliation: IRCCS-G.B. Bietti Eye Foundation, Rome, Italy.
authors.forename: Simona
authors.initials: S
authors.lastname: Minchiotti
authors.forename: Barbara
authors.initials: B
authors.lastname: Stampachiacchiere
authors.forename: Alessandra
authors.initials: A
authors.lastname: Micera
authors.forename: Alessandro
authors.initials: A
authors.lastname: Lambiase
authors.forename: Guido
authors.initials: G
authors.lastname: Ripandelli
authors.forename: Bernardo
authors.initials: B
authors.lastname: Billi
authors.forename: Stefano
authors.initials: S
authors.lastname: Bonini
mesh_terms: D000199:Actins / Q000378:metabolism; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D004797:Enzyme-Linked Immunosorbent Assay; D019773:Epiretinal Membrane / Q000235:genetics / Q000378:metabolism*; D005260:Female; D005347:Fibroblasts / Q000473:pathology; D019084:Fluorescent Antibody Technique, Indirect; D006801:Humans; D008297:Male; D008875:Middle Aged; D020932:Nerve Growth Factor / Q000235:genetics / Q000378:metabolism*; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism*; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D000077294:Receptor, Transforming Growth Factor-beta Type II; D020917:Receptor, trkA / Q000235:genetics / Q000378:metabolism*; D017475:Receptors, Nerve Growth Factor / Q000235:genetics / Q000378:metabolism*; D018125:Receptors, Transforming Growth Factor beta / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D053773:Transforming Growth Factor beta1 / Q000235:genetics / Q000378:metabolism; D014822:Vitreous Body / Q000378:metabolism
chemical_list: C541116:ACTA2 protein, human; D000199:Actins; C484065:NGFR protein, human; D009419:Nerve Tissue Proteins; D012333:RNA, Messenger; D017475:Receptors, Nerve Growth Factor; D018125:Receptors, Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; D020932:Nerve Growth Factor; D020917:Receptor, trkA; D017346:Protein Serine-Threonine Kinases; D000077294:Receptor, Transforming Growth Factor-beta Type II