Kohno R-i, Hata Y, Kawahara S, Kita T, Arita R, Mochizuki Y, Aiello L P, Ishibashi T
Department of Ophthalmology, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
Br J Ophthalmol. 2009 Aug;93(8):1020-6. doi: 10.1136/bjo.2008.155069. Epub 2009 May 7.
To address the cellular components and the contractile mechanisms of the idiopathic epiretinal membrane (ERM).
Ten surgically removed ERMs were fixed in 4% paraformaldehyde and analysed by whole-mount immunohistochemistry with anti-glial fibrillar acidic protein (GFAP) and alpha smooth-muscle actin (alphaSMA) antibodies. Type I collagen gel contraction assay, an established wound-healing assay in vitro, was performed using cultured bovine hyalocytes or normal human astrocytes (NHA) to evaluate the contractile property of the cells in the presence of tissue growth factor (TGF)-beta2. The expression of alphaSMA was also analysed by western blot analysis to examine myofibroblastic transdifferentiation of the cells. Vitreous-induced collagen gel contraction was also evaluated.
All membranes were composed of alphaSMA immunopositive cells in contracted foci and GFAP immunopositive cells in the periphery. No apparent double positive cells were observed in any membranes examined. Cultured hyalocytes showed overexpression of alphaSMA and hypercontraction of collagen gels in response to TGF-beta2, while glial cells showed marginal change. The vitreous from ERM patients also caused overexpression of alphaSMA and hypercontraction of the gels embedding hyalocytes, which were almost completely inhibited in the presence of anti-TGF-beta2 neutralising antibody.
Hyalocytes might be one of the critical components of ERM mediating its contractile property through the effect of TGF-beta2 in the vitreous fluid.
探讨特发性视网膜前膜（ERM）的细胞成分及收缩机制。
将10个手术切除的ERM用4%多聚甲醛固定，并用抗胶质纤维酸性蛋白（GFAP）和α平滑肌肌动蛋白（αSMA）抗体进行全层免疫组织化学分析。使用培养的牛玻璃体细胞或正常人星形胶质细胞（NHA）进行I型胶原凝胶收缩试验，这是一种已建立的体外伤口愈合试验，以评估在组织生长因子（TGF）-β2存在下细胞的收缩特性。还通过蛋白质印迹分析来分析αSMA的表达，以检测细胞的肌成纤维细胞转分化。同时评估玻璃体诱导的胶原凝胶收缩情况。
所有的膜在收缩灶中均由αSMA免疫阳性细胞组成，在外周由GFAP免疫阳性细胞组成。在所检查的任何膜中均未观察到明显的双阳性细胞。培养的玻璃体细胞在TGF-β2作用下显示αSMA过表达和胶原凝胶过度收缩，而胶质细胞则变化不明显。ERM患者的玻璃体也导致αSMA过表达和包埋玻璃体细胞的凝胶过度收缩，而在抗TGF-β2中和抗体存在的情况下，这种情况几乎完全受到抑制。
玻璃体细胞可能是ERM的关键成分之一，通过玻璃体中TGF-β2的作用介导其收缩特性。
