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Myo/Nog cells expressing muscle proteins are present in preretinal membranes from patients with proliferative vitreoretinopathy.
Experimental Eye Research ( IF 3.4 ) Pub Date : 2020-05-29 , DOI: 10.1016/j.exer.2020.108080
Jacquelyn Gerhart 1 , Nathan Morrison 1 , Lindsay Gugerty 1 , David Telander 2 , Arturo Bravo-Nuevo 1 , Mindy George-Weinstein 1
Affiliation  

Proliferative vitreoretinopathy (PVR) is a complication of rhegmatogenous retinal detachment and ocular trauma. The disease is characterized by development of membranes that may apply traction to the retina and cause redetachment. Membrane contractions are attributed to myofibroblasts arising from retinal pigment epithelial cells, glia and fibroblasts. The progenitors of myofibrobasts in the lens are Myo/Nog cells that express the skeletal muscle transcription factor MyoD and bone morphogenetic protein inhibitor Noggin. The retina and choroid also contain Myo/Nog cells that respond to stress. We examined preretinal PVR membranes from three ocular trauma patients with retinal detachment for Myo/Nog cells and their expression of muscle proteins. Myo/Nog cells were identified by co-localization of antibodies to the G8 antigen and Noggin. Greater than 80% of all cells in sections from two of three patients expressed both G8 and Noggin. Myo/Nog cells lacked pigment. Alpha smooth muscle actin (α-SMA) and striated myosin II heavy chain were present in the majority of Myo/Nog cells in these two patients. Differentiation of Myo/Nog cells was paralleled by low levels of MyoD. Membrane sections from the third patient consisted mostly of connective tissue with very few cells. A small subpopulation in these sections expressed both G8 and Noggin, and muscle proteins were detected in only a minority of G8-positive (+) cells. In all three patients, greater than 99% of cells with MyoD, α-SMA and striated muscle myosin co-expressed G8. These findings suggest that contractile myofibroblasts in PVR membranes may be derived from differentiating Myo/Nog cells.



中文翻译:

增生性玻璃体视网膜病变患者的视网膜前膜中存在表达肌肉蛋白的Myo / Nog细胞。

增生性玻璃体视网膜病变(PVR)是流源性视网膜脱离和眼外伤的并发症。该疾病的特征是膜的发育可能会向视网膜施加牵引力并引起再脱离。膜收缩归因于源自视网膜色素上皮细胞,神经胶质和成纤维细胞的成纤维细胞。晶状体中肌原纤维的祖细胞是表达骨骼肌转录因子MyoD和骨形态发生蛋白抑制剂Noggin的Myo / Nog细胞。视网膜和脉络膜也含有对压力有反应的Myo / Nog细胞。我们检查了三名视网膜脱离的眼外伤患者的视网膜前PVR膜的Myo / Nog细胞及其肌肉蛋白的表达。通过将针对G8抗原和Noggin的抗体共定位来鉴定Myo / Nog细胞。三分之二的患者中有超过80%的细胞切片同时表达了G8和Noggin。Myo / Nog细胞缺乏色素。这两名患者的大多数Myo / Nog细胞中均存在α平滑肌肌动蛋白(α-SMA)和横纹肌球蛋白II重链。Myo / Nog细胞的分化与低水平的MyoD平行。第三例患者的膜切片主要由结缔组织组成,细胞很少。这些部分中的一小部分亚群同时表达了G8和Noggin,并且仅在少数G8阳性(+)细胞中检测到了肌肉蛋白。在所有三名患者中,超过99%的MyoD,α-SMA和横纹肌肌球蛋白细胞共表达G8。这些发现表明,PVR膜中的收缩性成纤维细胞可能源自分化的Myo / Nog细胞。

更新日期:2020-05-29
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