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Exosomes derived from microglia exposed to elevated pressure amplify the neuroinflammatory response in retinal cells.
Glia ( IF 5.4 ) Pub Date : 2020-07-09 , DOI: 10.1002/glia.23880 Inês Dinis Aires 1, 2, 3 , Teresa Ribeiro-Rodrigues 1, 2, 3 , Raquel Boia 1, 2, 3 , Steve Catarino 1, 2, 3 , Henrique Girão 1, 2, 3 , António Francisco Ambrósio 1, 2, 3, 4 , Ana Raquel Santiago 1, 2, 3, 4
Glia ( IF 5.4 ) Pub Date : 2020-07-09 , DOI: 10.1002/glia.23880 Inês Dinis Aires 1, 2, 3 , Teresa Ribeiro-Rodrigues 1, 2, 3 , Raquel Boia 1, 2, 3 , Steve Catarino 1, 2, 3 , Henrique Girão 1, 2, 3 , António Francisco Ambrósio 1, 2, 3, 4 , Ana Raquel Santiago 1, 2, 3, 4
Affiliation
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Glaucoma is a degenerative disease that causes irreversible loss of vision and is characterized by retinal ganglion cell (RGC) loss. Others and we have demonstrated that chronic neuroinflammation mediated by reactive microglial cells plays a role in glaucomatous pathology. Exosomes are extracellular vesicles released by most cells, including microglia, that mediate intercellular communication. The role of microglial exosomes in glaucomatous degeneration remains unknown. Taking the prominent role of microglial exosomes in brain neurodegenerative diseases, we studied the contribution of microglial‐derived exosomes to the inflammatory response in experimental glaucoma. Microglial cells were exposed to elevated hydrostatic pressure (EHP), to mimic elevated intraocular pressure, the main risk factor for glaucoma. Naïve microglia (BV‐2 cells or retinal microglia) were exposed to exosomes derived from BV‐2 cells under EHP conditions (BV‐Exo‐EHP) or cultured in control pressure (BV‐Exo‐Control). We found that BV‐Exo‐EHP increased the production of pro‐inflammatory cytokines, promoted retinal microglia motility, phagocytic efficiency, and proliferation. Furthermore, the incubation of primary retinal neural cell cultures with BV‐Exo‐EHP increased cell death and the production of reactive oxygen species. Exosomes derived from retinal microglia (MG‐Exo‐Control or MG‐Exo‐EHP) were injected in the vitreous of C57BL/6J mice. MG‐Exo‐EHP sustained activation of retinal microglia, mediated cell death, and impacted RGC number. Herein, we show that exosomes derived from retinal microglia have an autocrine function and propagate the inflammatory signal in conditions of elevated pressure, contributing to retinal degeneration in glaucomatous conditions.
中文翻译：
来自暴露于高压的小胶质细胞的外泌体放大了视网膜细胞中的神经炎症反应。
青光眼是一种退行性疾病，会导致不可逆的视力丧失，其特征是视网膜神经节细胞 (RGC) 损失。其他人和我们已经证明，由反应性小胶质细胞介导的慢性神经炎症在青光眼病理中起作用。外泌体是由大多数细胞（包括小胶质细胞）释放的细胞外囊泡，可介导细胞间通讯。小胶质细胞外泌体在青光眼变性中的作用仍然未知。利用小胶质细胞外泌体在脑神经退行性疾病中的突出作用，我们研究了小胶质细胞衍生的外泌体对实验性青光眼炎症反应的贡献。小胶质细胞暴露于升高的静水压 (EHP)，以模拟升高的眼内压，这是青光眼的主要危险因素。幼稚小胶质细胞（BV-2 细胞或视网膜小胶质细胞）在 EHP 条件下（BV-Exo-EHP）暴露于源自 BV-2 细胞的外泌体，或在控制压力下培养（BV-Exo-Control）。我们发现 BV-Exo-EHP 增加了促炎细胞因子的产生，促进了视网膜小胶质细胞的运动、吞噬效率和增殖。此外，原代视网膜神经细胞培养物与 BV-Exo-EHP 的孵育增加了细胞死亡和活性氧的产生。将源自视网膜小胶质细胞的外泌体（MG-Exo-Control 或 MG-Exo-EHP）注射到 C57BL/6J 小鼠的玻璃体内。MG-Exo-EHP 持续激活视网膜小胶质细胞，介导细胞死亡，并影响 RGC 数量。在此处，
更新日期：2020-07-09
中文翻译：
来自暴露于高压的小胶质细胞的外泌体放大了视网膜细胞中的神经炎症反应。
青光眼是一种退行性疾病，会导致不可逆的视力丧失，其特征是视网膜神经节细胞 (RGC) 损失。其他人和我们已经证明，由反应性小胶质细胞介导的慢性神经炎症在青光眼病理中起作用。外泌体是由大多数细胞（包括小胶质细胞）释放的细胞外囊泡，可介导细胞间通讯。小胶质细胞外泌体在青光眼变性中的作用仍然未知。利用小胶质细胞外泌体在脑神经退行性疾病中的突出作用，我们研究了小胶质细胞衍生的外泌体对实验性青光眼炎症反应的贡献。小胶质细胞暴露于升高的静水压 (EHP)，以模拟升高的眼内压，这是青光眼的主要危险因素。幼稚小胶质细胞（BV-2 细胞或视网膜小胶质细胞）在 EHP 条件下（BV-Exo-EHP）暴露于源自 BV-2 细胞的外泌体，或在控制压力下培养（BV-Exo-Control）。我们发现 BV-Exo-EHP 增加了促炎细胞因子的产生，促进了视网膜小胶质细胞的运动、吞噬效率和增殖。此外，原代视网膜神经细胞培养物与 BV-Exo-EHP 的孵育增加了细胞死亡和活性氧的产生。将源自视网膜小胶质细胞的外泌体（MG-Exo-Control 或 MG-Exo-EHP）注射到 C57BL/6J 小鼠的玻璃体内。MG-Exo-EHP 持续激活视网膜小胶质细胞，介导细胞死亡，并影响 RGC 数量。在此处，
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