Human idiopathic epiretinal membranes express NGF and NGF receptors

PURPOSE: 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-β1 (TGF-β1) play a crucial role in FB activities. Therefore, the authors evaluated myoFBs in ERMs and NGF, trkA and p75 expression, as well as TGF-β1/TGF-βRII 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 α-smooth muscle actin (α-SMA, a defined myoFB marker), NGF, trkA/p75, and TGF-β1/TGF-βRII. RESULTS: Every idiopathic ERM displayed α-SMA positive myoFBs, expressing NGF, trkA, and p75. ERM vitreous showed a significant decrease in NGF protein coupled with a TGF-β1 increase. In addition, vitreous cells showed an increase in trkA/p75 mRNA associated with a decrease in TGF-βRII 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-β1, in the evolution and myoFB-mediated contractile activity of ERMs.