Gerhart Jacquelyn, Greenbaum Marvin, Scheinfeld Victoria, Fitzgerald Paul, Crawford Mitchell, Bravo-Nuevo Arturo, Pitts Meghan, George-Weinstein Mindy
Lankenau Institute for Medical Research, Wynnewood, Pennsylvania, United States of America.
Lankenau Medical Center, Wynnewood, Pennsylvania, United States of America.
PLoS One. 2014 Apr 15;9(4):e95262. doi: 10.1371/journal.pone.0095262. eCollection 2014.
Posterior capsule opacification (PCO) is a vision impairing condition that arises in some patients following cataract surgery. The fibrotic form of PCO is caused by myofibroblasts that may emerge in the lens years after surgery. In the chick embryo lens, myofibroblasts are derived from Myo/Nog cells that are identified by their expression of the skeletal muscle specific transcription factor MyoD, the bone morphogenetic protein inhibitor Noggin, and the epitope recognized by the G8 monoclonal antibody. The goal of this study was to test the hypothesis that depletion of Myo/Nog cells will prevent the accumulation of myofibroblasts in human lens tissue. Myo/Nog cells were present in anterior, equatorial and bow regions of the human lens, cornea and ciliary processes. In anterior lens tissue removed by capsulorhexis, Myo/Nog cells had synthesized myofibroblast and skeletal muscle proteins, including vimentin, MyoD and sarcomeric myosin. Alpha smooth muscle actin (α-SMA) was detected in a subpopulation of Myo/Nog cells. Areas of the capsule denuded of epithelial cells were surrounded by Myo/Nog cells. Some of these cell free areas contained a wrinkle in the capsule. Depletion of Myo/Nog cells eliminated cells expressing skeletal muscle proteins in 5-day cultures but did not affect cells immunoreactive for beaded filament proteins that accumulate in differentiating lens epithelial cells. Transforming growth factor-betas 1 and 2 that mediate an epithelial-mesenchymal transition, did not induce the expression of skeletal muscle proteins in lens cells following Myo/Nog cell depletion. This study demonstrates that Myo/Nog cells in anterior lens tissue removed from cataract patients have undergone a partial differentiation to skeletal muscle. Myo/Nog cells appear to be the source of skeletal muscle-like cells in explants of human lens tissue. Targeting Myo/Nog cells with the G8 antibody during cataract surgery may reduce the incidence of PCO.
后囊膜混浊（PCO）是一种在白内障手术后部分患者中出现的视力损害病症。PCO的纤维化形式是由成肌纤维细胞引起的，这些细胞可能在手术后数年出现在晶状体中。在鸡胚晶状体中，成肌纤维细胞源自Myo/Nog细胞，这些细胞通过其对骨骼肌特异性转录因子MyoD、骨形态发生蛋白抑制剂Noggin以及G8单克隆抗体识别的表位的表达来鉴定。本研究的目的是检验以下假设：Myo/Nog细胞的缺失将阻止人晶状体组织中肌成纤维细胞的积累。Myo/Nog细胞存在于人晶状体、角膜和睫状体的前部、赤道部和弓状区域。在通过撕囊术移除的前晶状体组织中，Myo/Nog细胞已合成了成肌纤维细胞和骨骼肌蛋白，包括波形蛋白、MyoD和肌节肌球蛋白。在Myo/Nog细胞的一个亚群中检测到α平滑肌肌动蛋白（α-SMA）。上皮细胞剥脱的囊膜区域被Myo/Nog细胞包围。这些无细胞区域中的一些在囊膜中有皱纹。在5天的培养中，Myo/Nog细胞的缺失消除了表达骨骼肌蛋白的细胞，但不影响对在分化的晶状体上皮细胞中积累的串珠状细丝蛋白具有免疫反应性的细胞。介导上皮-间充质转化的转化生长因子β1和β2在Myo/Nog细胞缺失后并未诱导晶状体细胞中骨骼肌蛋白的表达。本研究表明，从白内障患者移除的前晶状体组织中的Myo/Nog细胞已部分分化为骨骼肌。Myo/Nog细胞似乎是人晶状体组织外植体中骨骼肌样细胞的来源。在白内障手术期间用G8抗体靶向Myo/Nog细胞可能会降低PCO的发生率。
