自发永生化的非人灵长类 Müller 神经胶质细胞系是探索细胞疗法视网膜重编程机制的来源。

IF 4.5 2区 生物学 Q2 CELL BIOLOGY Journal of Cellular Physiology Pub Date : 2024-11-28 DOI:10.1002/jcp.31482
Ahmed Salman, Arantxa Bolinches-Amorós, Tina Storm, Daniela Moralli, Paulina Bryika, Angela J. Russell, Stephen G. Davies, Alun R. Barnard, Robert E. MacLaren
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引用次数: 0

摘要

由于原代细胞在培养过程中存活率低,因此针对以光感受器变性为特征的眼部疾病的细胞替代疗法具有挑战性。一种稳定的视网膜细胞来源有望取代失去的光感受器。缪勒神经胶质细胞为视网膜神经元提供新陈代谢和结构支持,防止光感受器异常迁移,并促进谷氨酸的安全摄取,在视网膜平衡中发挥着关键作用。在鱼类和两栖动物中,受伤的视网膜可通过类似 Müller 的神经胶质干细胞再生,而哺乳动物视网膜中却没有这种现象,原因不明。对 Müller 细胞的研究一直很复杂,因为很难获得纯细胞群,而且它们在培养过程中会迅速去分化。虽然描述了来自人类和大鼠的各种 Müller 胶质细胞系,但目前还没有非人灵长类动物的 Müller 胶质细胞系。在这里,我们报告了源自猕猴神经视网膜的自发永生化 Müller 胶质细胞系,它们对生长因子有反应,并能在培养过程中无限扩增。它们表现出Müller细胞的形态,如拉长的形状和胞质突起,表达Müller胶质细胞标记(VIMENTIN、谷氨酸合成酶、谷氨酸-天门冬氨酸转运体和CD44),并表达干细胞标记,如PAX6和SOX2。在存在诱导感光细胞分化的因子时,这些细胞的基因表达模式会发生变化,显示出一种去分化状态,这是哺乳动物Müller细胞中已知的一种重编程现象。自我更新视网膜的概念看似不可行,但并非史无前例。虽然脊椎动物的Müller胶质细胞具有哺乳动物所不具备的再生潜力,但了解哺乳动物Müller胶质细胞重编程背后的机制,可以释放它们治疗视网膜退行性疾病的潜力。
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Spontaneously Immortalised Nonhuman Primate Müller Glia Cell Lines as Source to Explore Retinal Reprogramming Mechanisms for Cell Therapies

Cell replacement therapies for ocular diseases characterised by photoreceptors degeneration are challenging due to poor primary cell survival in culture. A stable retinal cell source to replace lost photoreceptors holds promise. Müller glia cells play a pivotal role in retinal homoeostasis by providing metabolic and structural support to retinal neurons, preventing aberrant photoreceptors migration, and facilitating safe glutamate uptake. In fish and amphibians, injured retinas regenerate due to Müller-like glial stem cells, a phenomenon absent in the mammalian retina for unknown reasons. Research on Müller cells has been complex due to difficulties in obtaining pure cell population and their rapid de-differentiation in culture. While various Müller glia cell lines from human and rats are described, no nonhuman primate Müller glia cell line is currently available. Here, we report spontaneously immortalised Müller glia cell lines derived from macaque neural retinas that respond to growth factors and expand indefinitely in culture. They exhibit Müller cells morphology, such as an elongated shape and cytoplasmic projections, express Müller glia markers (VIMENTIN, GLUTAMINE SYNTHASE, glutamate-aspartate transporter, and CD44), and express stem cell markers such as PAX6 and SOX2. In the presence of factors that induce photoreceptor differentiation, these cells show a shift in gene expression patterns suggesting a state of de-differentiation, a phenomenon known in reprogrammed mammalian Müller cells. The concept of self-renewing retina might seem unfeasible, but not unprecedented. While vertebrate Müller glia have a regeneration potential absent in mammals, understanding the mechanisms behind reprogramming of Müller glia in mammals could unlock their potential for treating retinal degenerative diseases.

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来源期刊
CiteScore
14.70
自引率
0.00%
发文量
256
审稿时长
1 months
期刊介绍: The Journal of Cellular Physiology publishes reports of high biological significance in areas of eukaryotic cell biology and physiology, focusing on those articles that adopt a molecular mechanistic approach to investigate cell structure and function. There is appreciation for the application of cellular, biochemical, molecular and in vivo genetic approaches, as well as the power of genomics, proteomics, bioinformatics and systems biology. In particular, the Journal encourages submission of high-interest papers investigating the genetic and epigenetic regulation of proliferation and phenotype as well as cell fate and lineage commitment by growth factors, cytokines and their cognate receptors and signal transduction pathways that influence the expression, integration and activities of these physiological mediators. Similarly, the Journal encourages submission of manuscripts exploring the regulation of growth and differentiation by cell adhesion molecules in addition to the interplay between these processes and those induced by growth factors and cytokines. Studies on the genes and processes that regulate cell cycle progression and phase transition in eukaryotic cells, and the mechanisms that determine whether cells enter quiescence, proliferate or undergo apoptosis are also welcomed. Submission of papers that address contributions of the extracellular matrix to cellular phenotypes and physiological control as well as regulatory mechanisms governing fertilization, embryogenesis, gametogenesis, cell fate, lineage commitment, differentiation, development and dynamic parameters of cell motility are encouraged. Finally, the investigation of stem cells and changes that differentiate cancer cells from normal cells including studies on the properties and functions of oncogenes and tumor suppressor genes will remain as one of the major interests of the Journal.
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