Minchiotti Simona, Stampachiacchiere Barbara, Micera Alessandra, Lambiase Alessandro, Ripandelli Guido, Billi Bernardo, Bonini Stefano
IRCCS-G.B. Bietti Eye Foundation, Rome, Italy.
Retina. 2008 Apr;28(4):628-37. doi: 10.1097/IAE.0b013e31815ec275.
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.
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.
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.
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.
神经胶质细胞和成纤维细胞（FBs）在视网膜前膜（ERM）的发生和发展中起关键作用。由这些细胞产生的肌成纤维细胞（myoFBs）可导致ERM中出现肥厚性瘢痕和组织收缩。神经生长因子（NGF）和转化生长因子-β1（TGF-β1）在FB活性中起关键作用。因此，作者评估了ERM中的myoFBs以及NGF、trkA（NGFR和p75（NTR）的表达，以及ERM和玻璃体中TGF-β1/TGF-βRII的水平。
在因黄斑皱襞行玻璃体切除术时，从患者身上获取8个特发性ERM和玻璃体。10个对照玻璃体来自捐献者。进行生化和分子分析以鉴定α-平滑肌肌动蛋白（α-SMA，一种明确的肌成纤维细胞标志物）、NGF、trkA（NGFR）/p75（NTR）和TGF-β1/TGF-βRII。
每个特发性ERM均显示α-SMA阳性的肌成纤维细胞，表达NGF、trkA（NGFR）和p75（NTR）。ERM玻璃体中NGF蛋白显著减少，同时TGF-β1增加。此外，玻璃体细胞中trkA（NGFR）/p75（NTR）mRNA增加，而TGF-βRII mRNA减少。
特发性ERM的特征是肌成纤维细胞。局部肌成纤维细胞中NGF、trkA和p75的表达以及ERM玻璃体中NGF的变化表明，如先前报道的TGF-β1一样，NGF参与了ERM的演变和肌成纤维细胞介导的收缩活性。
