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Astrocyte Support for Oligodendrocyte Differentiation can be Conveyed via Extracellular Vesicles but Diminishes with Age.
Scientific Reports ( IF 3.8 ) Pub Date : 2020-01-21 , DOI: 10.1038/s41598-020-57663-x Cory M Willis 1 , Alexandra M Nicaise 1 , Ernesto R Bongarzone 2 , Maria Givogri 2 , Cory R Reiter 2 , Olivia Heintz 1 , Evan R Jellison 3 , Pearl A Sutter 1 , Gregg TeHennepe 4 , Guruprasad Ananda 4 , Anthony T Vella 3 , Stephen J Crocker 1
Scientific Reports ( IF 3.8 ) Pub Date : 2020-01-21 , DOI: 10.1038/s41598-020-57663-x Cory M Willis 1 , Alexandra M Nicaise 1 , Ernesto R Bongarzone 2 , Maria Givogri 2 , Cory R Reiter 2 , Olivia Heintz 1 , Evan R Jellison 3 , Pearl A Sutter 1 , Gregg TeHennepe 4 , Guruprasad Ananda 4 , Anthony T Vella 3 , Stephen J Crocker 1
Affiliation
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The aging brain is associated with significant changes in physiology that alter the tissue microenvironment of the central nervous system (CNS). In the aged CNS, increased demyelination has been associated with astrocyte hypertrophy and aging has been implicated as a basis for these pathological changes. Aging tissues accumulate chronic cellular stress, which can lead to the development of a pro-inflammatory phenotype that can be associated with cellular senescence. Herein, we provide evidence that astrocytes aged in culture develop a spontaneous pro-inflammatory and senescence-like phenotype. We found that extracellular vesicles (EVs) from young astrocyte were sufficient to convey support for oligodendrocyte differentiation while this support was lost by EVs from aged astrocytes. Importantly, the negative influence of culture age on astrocytes, and their cognate EVs, could be countered by treatment with rapamycin. Comparative proteomic analysis of EVs from young and aged astrocytes revealed peptide repertoires unique to each age. Taken together, these findings provide new information on the contribution of EVs as potent mediators by which astrocytes can extert changing influence in either the disease or aged brain.
中文翻译：
星形胶质细胞对少突胶质细胞分化的支持可以通过细胞外囊泡传递，但随着年龄的增长而减少。
大脑衰老与生理机能的重大改变有关，后者改变了中枢神经系统（CNS）的组织微环境。在衰老的中枢神经系统中，脱髓鞘增加与星形胶质细胞肥大有关，衰老被认为是这些病理改变的基础。衰老的组织会积聚慢性细胞应激，这会导致促炎表型的发展，这种表型可能与细胞衰老有关。在本文中，我们提供证据表明，在培养物中老化的星形胶质细胞会自发形成促炎和衰老样表型。我们发现年轻星形胶质细胞的细胞外囊泡（EVs）足以为少突胶质细胞分化提供支持，而这种支持却被老化的星形胶质细胞的EVs失去了。重要的是，培养年龄对星形胶质细胞的负面影响，其雷同的电动汽车可以通过雷帕霉素治疗来对抗。对来自年轻和老年星形胶质细胞的电动汽车进行的蛋白质组学比较分析显示，每个年龄段都有独特的肽库。综上所述，这些发现提供了有关电动汽车作为有效介质的贡献的新信息，通过这些介质，星形胶质细胞可以在疾病或衰老的大脑中发挥不断变化的影响。
更新日期：2020-01-22
中文翻译：
星形胶质细胞对少突胶质细胞分化的支持可以通过细胞外囊泡传递，但随着年龄的增长而减少。
大脑衰老与生理机能的重大改变有关，后者改变了中枢神经系统（CNS）的组织微环境。在衰老的中枢神经系统中，脱髓鞘增加与星形胶质细胞肥大有关，衰老被认为是这些病理改变的基础。衰老的组织会积聚慢性细胞应激，这会导致促炎表型的发展，这种表型可能与细胞衰老有关。在本文中，我们提供证据表明，在培养物中老化的星形胶质细胞会自发形成促炎和衰老样表型。我们发现年轻星形胶质细胞的细胞外囊泡（EVs）足以为少突胶质细胞分化提供支持，而这种支持却被老化的星形胶质细胞的EVs失去了。重要的是，培养年龄对星形胶质细胞的负面影响，其雷同的电动汽车可以通过雷帕霉素治疗来对抗。对来自年轻和老年星形胶质细胞的电动汽车进行的蛋白质组学比较分析显示，每个年龄段都有独特的肽库。综上所述，这些发现提供了有关电动汽车作为有效介质的贡献的新信息，通过这些介质，星形胶质细胞可以在疾病或衰老的大脑中发挥不断变化的影响。
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