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首页> 外文期刊>Neuroscience: An International Journal under the Editorial Direction of IBRO >EXACERBATED INFLAMMATORY RESPONSES RELATED TO ACTIVATED MICROGLIA AFTER TRAUMATIC BRAIN INJURY IN PROGRANULIN-DEFICIENT MICE
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EXACERBATED INFLAMMATORY RESPONSES RELATED TO ACTIVATED MICROGLIA AFTER TRAUMATIC BRAIN INJURY IN PROGRANULIN-DEFICIENT MICE

机译：乳蛋白缺乏症小鼠创伤性脑损伤后活化小胶质细胞的炎症反应

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Progranulin (PGRN), a multifunctional growth factor, appears to play a role in neurodegenerative diseases accompanied by neuroinflammation. In this study, we investigated the role of PGRN in neuroinflammation, especially in the activation of microglia, by means of experimental traumatic brain injury (TBI) in the cerebral cortex of mice. The expression of GRN mRNA was increased in association with neuroinflammation after TBI. Double-immunohistochemical study showed that PGRN-immunoreactive (-IR) cells were mainly overlapped with CD68-IR cells, suggesting that the main source of PGRN was CD68-positive activated microglia. To investigate the role of PGRN in inflammatory responses related to activated microglia, we compared the immunoreactivity and expression of ionized calcium-binding adaptor molecule 1 (Iba1), CD68, and CD11b as markers for activated microglia between wild-type (WT) and GRN-deficient (KO) mice. The number of Iba1- and CD11b-IR cells and gene expression of Iba1 and CDUbwere not significantly different between WT and KO mice, while the number of CD68-IR cells and CD68 expression in KO mice were significantly greater than those in WT mice. Double-immunohistochemical study showed that CD68-IR microglia were also IR for TGFpi, and TGFpi expression and Smad3 phosphorylation in KO mice were elevated compared to WT mice. Moreover, double-immunostaining between phospho-Smad3 and glial fibrillary acidic protein suggested increased TGFp1-Smad3 signal mainly by astrocytes. The levels of protein carbonyl groups, which reflect protein oxidation, and laminin immunoreactivity, which is associated with angiogenesis, were also significantly increased in KO mice compared to WT mice. These results suggest that PGRN is produced in CD68-positive microglia and suppresses excessive inflammatory responses related to activated microglia after TBI in mice.
机译：前颗粒蛋白（PGRN）是一种多功能生长因子，似乎在伴随神经发炎的神经退行性疾病中起作用。在这项研究中，我们通过小鼠大脑皮质的实验性脑损伤（TBI），研究了PGRN在神经炎症，特别是在小胶质细胞活化中的作用。 TBI后GRN mRNA的表达与神经炎症相关。双重免疫组织化学研究显示，PGRN免疫反应性（-IR）细胞主要与CD68-IR细胞重叠，表明PGRN的主要来源是CD68阳性活化的小胶质细胞。为了研究PGRN在与活化的小胶质细胞相关的炎症反应中的作用，我们比较了野生型（WT）和GRN之间电离钙结合衔接子分子1（Iba1），CD68和CD11b作为活化的小胶质细胞的标志物的免疫反应性和表达缺陷（KO）小鼠。 WT和KO小鼠之间的Iba1-和CD11b-IR细胞数量以及Iba1和CDUb的基因表达没有显着差异，而KO小鼠中的CD68-IR细胞数量和CD68表达明显高于WT小鼠。双重免疫组织化学研究显示，CD68-IR小胶质细胞对TGFpi也具有IR，与WT小鼠相比，KO小鼠中TGFpi表达和Smad3磷酸化升高。此外，磷酸化Smad3和胶质纤维酸性蛋白之间的双重免疫染色提示TGFp1-Smad3信号主要由星形胶质细胞引起。与野生型小鼠相比，KO小鼠中反映蛋白质氧化的蛋白质羰基水平和层粘连蛋白免疫反应性（与血管生成相关）也显着增加。这些结果表明，PGRN在CD68阳性小胶质细胞中产生，并抑制了小鼠TBI后与活化的小胶质细胞相关的过度炎症反应。

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