Nakamoto Chizu, Kuan Soh-Leh, Findlay Amy S, Durward Elaine, Ouyang Zhufeng, Zakrzewska Ewa D, Endo Takuma, Nakamoto Masaru
Aberdeen Developmental Biology Group, School of Medical Sciences, University of Aberdeen, Aberdeen AB25 2ZD, United Kingdom Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, and Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH 44195.
Mol Biol Cell. 2014 Jan;25(2):234-44. doi: 10.1091/mbc.E13-08-0453. Epub 2013 Nov 20.
For correct functioning of the nervous system, the appropriate number and complement of neuronal cell types must be produced during development. However, the molecular mechanisms that regulate the production of individual classes of neurons are poorly understood. In this study, we investigate the function of the thrombospondin-1-like glycoprotein, Nel (neural epidermal growth factor [EGF]-like), in the generation of retinal ganglion cells (RGCs) in chicks. During eye development, Nel is strongly expressed in the presumptive retinal pigment epithelium and RGCs. Nel overexpression in the developing retina by in ovo electroporation increases the number of RGCs, whereas the number of displaced amacrine cells decreases. Conversely, knockdown of Nel expression by transposon-mediated introduction of RNA interference constructs results in decrease in RGC number and increase in the number of displaced amacrine cells. Modifications of Nel expression levels do not appear to affect proliferation of retinal progenitor cells, but they significantly alter the progression rate of RGC differentiation from the central retina to the periphery. Furthermore, Nel protects RGCs from apoptosis during retinal development. These results indicate that Nel positively regulates RGC production by promoting their differentiation and survival during development.
为使神经系统正常运作,发育过程中必须产生适当数量和种类的神经元细胞。然而,调节各类神经元产生的分子机制目前仍知之甚少。在本研究中,我们探究了血小板反应蛋白-1样糖蛋白Nel(神经表皮生长因子[EGF]样)在雏鸡视网膜神经节细胞(RGC)生成中的作用。在眼睛发育过程中,Nel在假定的视网膜色素上皮和RGC中强烈表达。通过卵内电穿孔在发育中的视网膜中过表达Nel会增加RGC的数量,而移位无长突细胞的数量则会减少。相反,通过转座子介导引入RNA干扰构建体来敲低Nel的表达会导致RGC数量减少,移位无长突细胞数量增加。Nel表达水平的改变似乎并不影响视网膜祖细胞的增殖,但它们会显著改变RGC从视网膜中央向周边分化的进程。此外,Nel在视网膜发育过程中保护RGC免受凋亡。这些结果表明,Nel通过在发育过程中促进RGC的分化和存活来正向调节RGC的产生。